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Yr2 Lily BRS Gastro > Upper GI tract disorders > Flashcards

Upper GI tract disorders Flashcards

1
Q

what is an overview of the anatomy of the oesophagus?

A

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

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2
Q

how is the lower oesophageal sphincter formed?

A

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)

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3
Q

what are the four phases of swallowing?

A

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)

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4
Q

what is the motility of the oesophagus like and how is it determined?

A

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)

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5
Q

what are possible causes of an absence of a stricture in the oesophagus?

A

Abnormal oesophageal contraction:
Hypermotility (eg. achalasia)
Hypomotility (eg. scleroderma)
Disordered coordination (eg. corkscrew oesophagus)

Failure of protective mechanisms for reflux:
GastroOesophageal Reflux Disease (GORD)

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6
Q

what is the meaning of dysphagia?

A

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

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7
Q

what is the meaning of odynophagia?

A

pain on swallowing

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8
Q

what is the meaning of regurgitation?

A

return of oesophageal contents from above an obstruction

May be functional or mechanical

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9
Q

what is the meaning of reflux?

A

passive return of gastroduodenal contents to the mouth

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10
Q

what is achalasia?

A

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)

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11
Q

what are the different types of achalasia and their causes?

A

Primary :
aetiology unknown

Secondary:
Diseases causing oesophageal motor abnormalities similar to primary achalasia -
Chagas’ Disease
Protozoa infection
Amyloid/Sarcoma/Eosinophilic Oesophagitis

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12
Q

what happens to swallowing in achalasia?

A

↑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

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13
Q

what are symptoms and progression of achalasia?

A

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%

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14
Q

how is achalasia treated?

A

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)

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15
Q

what is scleroderma?

A

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)

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16
Q

how is scleroderma treated?

A

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

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17
Q

what is corkscrew oesophagus?

A

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
18
Q

how is corkscrew oesophagus treated?

A

May respond to forceful PD (pneumatic dilatation) of cardia

Results not as predictable as achalasia

19
Q

what are the areas of constriction in the oesophagus?

A

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)

20
Q

what is the aetiology of oesophageal perforation?

A 
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

21
Q

what are the iatrogenic causes of oesophageal perforation?

A

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%
22
Q

what it boerhaaves?

A

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

23
Q

what foreign bodies may cause oesophageal perforation?

A

Disk batteries growing problem
Cause electrical burns if embeds in mucosa

Magnets

Sharp objects

Dishwasher tablets

Acid/Alkali

24
Q

how does trauma cause oesophageal perforation?

A 
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)
25
Q

how do oesophageal perforations present?

A

Pain 95 %
Fever 80 %
Dysphagia 70 %
Emp(h?)ysema 35 %

oesophageal and gastric contents may enter the lungs (Pleural effusion)

26
Q

what investigations are done for oesophageal perforations?

A

chest x ray
CT
swallow (gastrograffin - contrast
OGD

27
Q

how are oesophageal perforations managed primarily?

A 
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
28
Q

how are oesophageal perforations treated?

A

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

29
Q

what increases and decreases the pressure of the lower oesophageal sphincter?

A

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

30
Q

what are the protective mechanisms of the oesophagus agains reflux?

A

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

31
Q

why might the protective mechanisms against reflux in the oesophagus fail?

A

(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

32
Q

what investigations are done for GORD (due to failure of protective mechanisms)

A

OGD
To exclude cancer
Oesophagitis, peptic stricture & Barretts oesophagus confirm ∆

Oesophageal manometry

24-hr oesophageal pH recording

33
Q

how is GORD treated?

A

Medical:
Lifestyle changes (wt loss, smoking, drinking)
PPIs

Surgical:
Dilatation peptic strictures
Laparoscopic Nissen’s fundoplication

34
Q

what are the functions of the stomach?

A

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

35
Q

what are the causes of different types of gastritis?

A

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

36
Q

what are the different types of gastritis?

A

erosive and haemorrhagic

nonerosive, chronic active

atrophic (fundal gland)

reactive

37
Q

how are gastric secretions regulated?

A

(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)
38
Q

how is the stomach protected from ulcers?

A

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))

39
Q

how is the stomachs epithelium repaired?

A

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.

40
Q

what causes stomach ulcer formation?

A

helicobacter pylori

increased secretion of gastric juice

decreased bicarbonate secretion

decreased cell formation

decreased blood perfusion

may be due to stress
or non steroidals

41
Q

how does H. pylori cause ulcers?

A

80% are asymptomatic or just cause chronic gastritis

15-20% Chronic atrophic gastritis
Intestinal metaplasia
Gastric or duodenal ulcer

<1% Gastric cancer
MALT lymphoma

42
Q

how are ulcers treated?

A

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

Yr2 Lily BRS Gastro (7 decks)

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