Upper GI tract disorders Flashcards
what is an overview of the anatomy of the oesophagus?
upper oesophageal sphincter at top (level with C5)
lower oesophageal sphincter at bottom (level with T10)
split into thirds:
1/3 - skeletal muscle
2/3 - skeletal and smooth muscle
3/3 - smooth muscle
lies behind:
trachea at top
aorta below
passes through the diaphragm
how is the lower oesophageal sphincter formed?
it is physiological - not an actual sphincter
Anatomical contributions to LOS:
3-4 cm distal oesophagus within abdomen
Diaphragm surrounds LOS (Lt & Rt crux)
An intact phrenoesophageal ligament (Extension of inferior diaphragmatic fascia”) (allows movement of the diaphragm and oesophagus separately)
Angle of His (angle between cardia at entrance of stomach and oesophagus)
what are the four phases of swallowing?
Stage 0: Oral phase
Chewing & saliva prepare bolus
Both oesophageal sphincters constricted
Stage 1: Pharyngeal phase
Pharyngeal musculature guides food bolus towards oesophagus
Upper oesophageal sphincter opens reflexly
LOS opened by vasovagal reflex (receptive relaxation reflex)
Stage 2: Upper oesophageal phase
Upper sphincter closes
Superior circular muscle rings contract & inferior rings dilate
Sequential contractions of longitudinal muscle
Stage 3: Lower oesophageal phase
Lower sphincter closes as food passes through
(both closed, both open top closes, bottom closes)
what is the motility of the oesophagus like and how is it determined?
determined using manometry - pressure measurements done by sticking a tube down it
Peristaltic waves ~ 40 mmHg
LOS resting pressure ~ 20 mmHg
↓<5 mmHg during receptive relaxation (this makes its pressure less than the stomach so food passes through)
Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus
(there is also a transient increase in its pressure after this)
what are possible causes of an absence of a stricture in the oesophagus?
Abnormal oesophageal contraction:
Hypermotility (eg. achalasia)
Hypomotility (eg. scleroderma)
Disordered coordination (eg. corkscrew oesophagus)
Failure of protective mechanisms for reflux:
GastroOesophageal Reflux Disease (GORD)
what is the meaning of dysphagia?
difficulty in swallowing.
Localisation is important – cricopharyngeal sphincter or distal
Type of dysphagia:
For solids or fluids
Intermittent or progressive
Precise or vague in appreciation
what is the meaning of odynophagia?
pain on swallowing
what is the meaning of regurgitation?
return of oesophageal contents from above an obstruction
May be functional or mechanical
what is the meaning of reflux?
passive return of gastroduodenal contents to the mouth
what is achalasia?
hypermotility of the oesophagus
Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
:. ↓ed activity of inhibitory NCNA neurones.
So loss of reflexive relaxation (vasovagal reflex)
what are the different types of achalasia and their causes?
Primary :
aetiology unknown
Secondary:
Diseases causing oesophageal motor abnormalities similar to primary achalasia -
Chagas’ Disease
Protozoa infection
Amyloid/Sarcoma/Eosinophilic Oesophagitis
what happens to swallowing in achalasia?
↑ed resting pressure of LOS (due to lack of inhibition)
Receptive relaxation sets in late & is too weak
During reflex phase pressure in LOS is markedly ↑er than stomach
Swallowed food collects in oesophagus causing ↑ pressure throughout with dilation of the oesophagus
Propagation of peristaltic waves cease
what are symptoms and progression of achalasia?
weight loss
trouble swallowing
pain
->oesophagitis, pneumonia from aspirating oesophageal contents
Disease Course:
Has insidious onset - symptoms for years prior to seeking help
Without treatment → progressive oesophageal dilatation of oesophagus.
Risk of oesophageal cancer ↑ed 28-fold
annual incidence only 0.34%
how is achalasia treated?
pneumatic dilatation (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
uses a balloon
OR
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
Risks:
Oesophageal & gastric perforation (10 – 16%)
Division of vagus nerve – rare
Splenic injury – 1 – 5% (as spleen is attached to stomach by short gastric arteries)
what is scleroderma?
Hypomotility of the oesophagus
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.
↓ed resting pressure of LOS
→ gastroesophageal reflux disease develops. (GORD)
Often associated with CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia)
how is scleroderma treated?
Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs → usually irreversible
what is corkscrew oesophagus?
an example of a disease due to disordered coordination of the oesophagus
Diffuse oesophageal spasm Incoordinate contractions → dysphagia & chest pain Pressures of 400-500 mmHg (should be 40) Marked hypertrophy of circular muscle Corkscrew oesophagus on Barium
how is corkscrew oesophagus treated?
May respond to forceful PD (pneumatic dilatation) of cardia
Results not as predictable as achalasia
what are the areas of constriction in the oesophagus?
3x areas of anatomical constriction:
cricopharyngeal (UOS)
aortic and bronchial
diaphragmatic and sphincter constriction (LOS)
may also be Pathological narrowing (cancer, foreign body, physiological dysfunction)
what is the aetiology of oesophageal perforation?
Iatrogenic (OGD (gastroscopy)) >50% Spontaneous (Boerhaave’s) - 15% Foreign body - 12% Trauma - 9% Intraoperative - 2% Malignant - 1%
more likely to happen where there are strictures
what are the iatrogenic causes of oesophageal perforation?
Usually at OGD (oesophago-gastro-duodenoscopy)
More common in presence of diverticula or cancer
Incidence: OGD = 0.03% Stricture dilatation = 0.1-2% Sclerotherapy = 1-5% Achalasia dilatation = 2-6%
what it boerhaaves?
a cause of oesophageal perforations, spontaneous perforations
Sudden ↑ in intra-oesophageal pressure with negative intra thoracic pressure (eg during vomiting)
Vomiting against a closed glottis
3.1 per 1,000,000
often on the Left posterolateral aspect of the distal oesophagus
what foreign bodies may cause oesophageal perforation?
Disk batteries growing problem
Cause electrical burns if embeds in mucosa
Magnets
Sharp objects
Dishwasher tablets
Acid/Alkali
how does trauma cause oesophageal perforation?
Neck = penetrating would Thorax = blunt force
Can be difficult to diagnose: Dysphagia Blood in saliva Haematemesis Surgical empysema (presence of gas in the subcutaneous soft tissues, crackling when you touch it)
how do oesophageal perforations present?
Pain 95 %
Fever 80 %
Dysphagia 70 %
Emp(h?)ysema 35 %
oesophageal and gastric contents may enter the lungs (Pleural effusion)
what investigations are done for oesophageal perforations?
chest x ray
CT
swallow (gastrograffin - contrast
OGD
how are oesophageal perforations managed primarily?
Surgical emergency (2x ↑mortality if 24h delay in diagnosis)
Initial management: NBM (nil by mouth) IV fluids Broad spectrum A/Bs & Antifungals ITU/HDU level care Bloods (including G&S) Tertiary referral centre
how are oesophageal perforations treated?
Conservative management with covered metal stent
(doesnt always work)
Operative management should be default:
Primary repair is optimal (stitch the layers of the oesophagus shut)
Oesophagectomy - definitive solution, rarer
what increases and decreases the pressure of the lower oesophageal sphincter?
LOS usually closed as barrier against reflux of harmful gastric juice (pepsin & HCl)
LOS pressure is increased by:
acetylcholine, alpha adrinergic agonists, hormones, protein rich foods, histamine, high intra abdominal pressure
LOS pressure is decreased by:
beta adrinergic agonists, hormones, dopamin, NO, chocolate, acid gastric juice, fat, smoking
what are the protective mechanisms of the oesophagus agains reflux?
LOS usually closed as barrier against reflux of harmful gastric juice (pepsin & HCl)
3x mechanisms protect following reflux:
Volume clearance - oesophageal peristalsis reflex (Pressure rises after reflux)
pH clearance - saliva
Epithelium - barrier properties
why might the protective mechanisms against reflux in the oesophagus fail?
(leads to GORD)
decreased sphincter pressure
transient sphincter opening (eg. due to fizzy drinks)
decreased saliva production (sleep, xerostomia)
decreased buffering capacity of saliva (eg. from smoking)
abnormal peristalsis (less volume clearance)
hiatus hernia (sliding or rolling (rolling is an emergency))
defective mucosal protective mechanism (eg. due to alcohol)
leads to:
reflux oesophagitis ->
oesophageal metaplasia ->
carcinoma
what investigations are done for GORD (due to failure of protective mechanisms)
OGD
To exclude cancer
Oesophagitis, peptic stricture & Barretts oesophagus confirm ∆
Oesophageal manometry
24-hr oesophageal pH recording
how is GORD treated?
Medical:
Lifestyle changes (wt loss, smoking, drinking)
PPIs
Surgical:
Dilatation peptic strictures
Laparoscopic Nissen’s fundoplication
what are the functions of the stomach?
Breaks food into smaller particles (acid & pepsin)
Holds food, releasing it in controlled steady rate into duodenum
Kills parasites & certain bacteria
Cardia & Pyloric Region: Mucus only
Body & Fundus: Mucus, HCl, pepsinogen
Antrum: Gastrin
what are the causes of different types of gastritis?
Erosive & haemorrhagic gastritis:
Numerous causes (eg. non steroidals)
Acute ulcer – gastric bleeding & perforation
Nonerosive, chronic active gastritis:
Antrum
Helicobacter pylori - Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14/7
Atrophic (fundal gland) gastritis:
Fundus
Autoantibodies vs parts & products of parietal cells
Parietal cells atrophy
↓acid & IF secretion
also leads to B12 deficiency and pernicious anaemia
reactive gastritis
what are the different types of gastritis?
erosive and haemorrhagic
nonerosive, chronic active
atrophic (fundal gland)
reactive
how are gastric secretions regulated?
(secretions of HCL-parietal cells, pepsinogen-chief cells)
STIMULATION
Neural:
ACh - postganglionic transmitter of vagal parasympathetic fibres
Endocrine :
Gastrin (G cells of antrum)
Paracrine :
Histamine (ECL cells & mast cells of gastric wall).
INHIBITION Endocrine: Secretin (small intestine) Paracrine: Somatostatin (SIH) Paracrine & autocrine: PGs (E2 & I2), TGF-α & adenosine (non steroidals decrease these)
how is the stomach protected from ulcers?
mucus film
bicarbonate secretion (requires prostaglandins, non steroidals prevent this through the COX pathway) acts as a buffer
epithelial barrier
mucosal blood perfusion, removes hydrogen ions (Sodium hydrogen exchange at basolateral end ( why protection is decreased in ischaemia))
how is the stomachs epithelium repaired?
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 causes stomach ulcer formation?
helicobacter pylori
increased secretion of gastric juice
decreased bicarbonate secretion
decreased cell formation
decreased blood perfusion
may be due to stress
or non steroidals
how does H. pylori cause ulcers?
80% are asymptomatic or just cause chronic gastritis
15-20% Chronic atrophic gastritis
Intestinal metaplasia
Gastric or duodenal ulcer
<1% Gastric cancer
MALT lymphoma
how are ulcers treated?
Primarily medical:
PPI or H2 blocker
Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)
Elective Surgical treatment:
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
Surgical indications Intractability (after medical therapy) Relative: continuous requirement of steroid therapy/NSAIDs Complications Haemorrhage Obstruction Perforation
