Oesophaguess the answer Flashcards

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1
Q

What sort of muscle type’s lines the Oesophagus?
Where are they located?
What part of the CNS controls the swallowing reflex?

A
Striated and smooth muscle
Upper 1/3 = striated 
Middle 1/3 = both
Lower 1/3 = smooth 
Medulla controls swallowing
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2
Q

What 3 physiological factors prevent reflux occurring?

A

1: LOS - intrinsic and diaphragmatic crura
2: Intra-abdominal oesophagus - pinch valve effect
3: Angle of entry of oesophagus into stomach

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3
Q

How is oesophageal dysphagia classified?

give an example of each

A

Solids only vs liquids + solids
Solids = mechanical obstruction, e.g. stricture or carcinoma
Both = neuromuscular disorder, e.g. diffuse oesophageal spasm, achalasia or scleroderma

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4
Q

How is Oropharyngeal dysphagia classified?

2 examples of each

A

Neurological - bulbar palsy, peripheral nerve palsy
Muscular - muscular dystrophy, polymyositis
Structural - Zenker’s diverticulum, thyromegaly

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5
Q

What is the pathophysiology behind Achalasia?

Etiology?

A

Inflammatory degeneration of Auerbach’s plexus -> increase in LES pressure -> incomplete relaxation of LES with swallowing -> aperistalsis
Etiology = idiopathic or secondary to malignancy

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6
Q

How is Achalasia diagnosed? Definitively?
What is its treatment?
Stats for treatment?
Severe risk of non-treatment?

A

Dx = CXR with no air in stomach, dilated oesophagus + Barium swallow with narrowing at LES ‘birds beak’ + endoscopy normal mucosa
- Manometry = definitive diagnosis
Tx = dilation of LES with 30-40mm balloon + PPI’s OR myotomy
Stats = 50% good response, risk of perforation 5%
Risk = SCC

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7
Q

What is the pathophysiology behind Scleroderma dysphagia?

A

Blood vessel damage -> intramural neuronal dysfunction -> distal oesophageal muscle weakening -> aperistalsis & loss of LES tone -> reflux -> stricture

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8
Q

How is Scleroderma diagnosed?

What is its treatment?

A
Dx = Clinical features of scleroderma + Manometry shows decreased pressure in LES + decreased peristalsis 
Tx = medical - PPI's bid, surgery - gastroplasty (last resort)
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9
Q

What is the pathophysiology behind Diffuse Oesophageal spasm?

A

Potential mechanisms include impaired inhibitory innervation to oesphageal body, malfunction in endogenous NO synthesis causing decreased relaxation

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10
Q

How is Diffuse Oesophageal Spasm diagnosed?

What is its treatment?

A

DxBarium swallowing with “corkscrew pattern” + Manometry has >30% but <100% of contractions are aperistaltic + endoscopy normal mucosa
Tx = reassure non-cardiac pain + nitrates, Calcium channel blockers or anti-cholinergics + long oesophageal myotomy if unresponsive +/- balloon dilation

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11
Q

What are 3 causes of odynophagia?

What are 3 swallowing techniques?

A
Causes = Mucosal inflammation (GORD), Hypertensive peristalsis + Malignancy 
techniques = chin tuck, head turning, forceful swallowing
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12
Q

What is the role of hiatus hernia’s on GORD?
What is the most common cause?
Most sensitive and specifIc signs for GORD?

A

Worsens reflux, but does not cause it
Most common = transient relaxation of LOS
Heartburn (pyrosis) and regurgitation

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13
Q

What are 5 food types that aggravate GORD?

What is an iatrogenic cause of GORD?

A

EtOH, Caffeine, Tobacco, Chocolate, spicy foods

Iatrogenic = post-surgical stress

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14
Q

What are the 3 types of drugs used to treat GORD?
Example of each
Mechanism of action

A

Acid suppressors - whatever - neutralise gastric acid
H2 receptor blockers - ranitidine - block histamine receptor of gastric parietal cells
PPI’s - omeprazole - inhibit the H+/K+ ATP pump

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15
Q

What are some extra-abdominal features of Crohn’s?

A

Anal skin tags
Iritis
Skin rash

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16
Q

What is an acute upper GIT complication of chronic liver disease?
Why does this occur?
What percentage will this spontaneously stop in?

A

Oesophageal varices haemorrhage
Due to cirrhosis of the liver causing shunting of portal vein blood into peripheral vasculature
50% will spontaneously stop

17
Q

Opposite which tooth is the opening of the parotid duct?
What 3 structures pass through here?
What is the innervation?

A

2nd upper molar
Facial nerve, external carotid artery & retromandibular vein (superficial temporal & maxillary veins)
Parasympathetic = glossopharyngeal + otic ganglion -> auriculotemporal nerve
Sympathetic = superior cervical ganglion

18
Q

Painful mouth ulcers, red halo’s found on inside of cheeks & lips
What are these?
What disease’s are associated with these signs?

A

Aphthous stomatitis

Coeliac, IBD & reactive arthritis

19
Q

What are 5 important questions to ask for dysphagia?

One disease for each

A
  • Solids, liquids or both? both = motility, solid = stricture
  • Difficulty actual swallowing motion? bulbar palsy
  • Intermittent or worsening? intermittent = spasm, worsening = cancer
  • Painful? ulceration
  • Gurgling sound and neck bulge? pharyngeal pouch
20
Q

What is Mallory-Weiss syndrome?
What are the two most common risk factors?
What is used for diagnosis, investigation and treatment?
What is the treatment?

A

Mucosal lacerations in the distal oesophagus and proximal stomach secondary to a sudden increase in intra-abdominal pressure
Alcohol use and hiatus hernia
Upper endoscopy
Treatment = Endoscopic repair + acid suppression (omeprazole 20mg OD 2wks)

21
Q

Barrett’s oesophagus pathophysiology?

Diagnosis?

A

Chronic acid reflux causing intestinal columnar metaplastic changes
Endoscopy documenting columnar epithelium in distal oesophagus + histoscopic signs of specialised intestinal metaplasia
Radio frequency ablation +/- endoscopic resection or fundoplication + high dose PPI’s

22
Q

Severe malnutrition followed by nasogastric nutrition - what metabolic symptom is likely to develop?

A

Hypophosphataemia

23
Q

What is the presentation/epidemiology of Zollinger-Ellison syndrome?
What is the best screening tool?
What other test can be used? What is diagnostic in this test?
What is the gastric pH?

A

Dyspepsia, fatigue and loss of weight in males aged between 20-50yrs old, multiple ulceration resistant to acid suppression
Screening = fasting serum gastrin
other = secretin stimulation test, gastrin levels >200pg/mL
pH = <2

24
Q

What conditions, other than coeliac disease, is sub-total villous atrophy seen?

A
Gastroenteritis
Whipple's disease 
Laxative abuse
Neomycin therapy 
Cow's milk/soya sensitivity in children
25
Q

What are 4 poor prognostic features of someone presenting with haematemesis?

A

Age >70
Signs of shock
Adherent clot or visible vessel on endoscopic examination
Co-morbidities

26
Q

What is Chilaiditi’s syndrome?

A

Normal variation causing bowel to be interposed between the liver and the right hemi-diaphragm

27
Q

What are some of the signs and symptoms that Whipple’s disease presents with?

A
Diarrhoea
Abdo pain
Lymphadenopathy
Fever
Weight loss
Arthritis
28
Q

What age do oesophageal carcinoma’s usually present?
M vs F incidence?
How do they differ according to site on oesophagus?
If resectable, what is needed next?

A
50-70yr old
M = F
Upper 1/3 = squamous carcinomas
Lower 2/3 = adenocarcinomas
Resectable = CT and endoscopic ultrasound + MDT assessment
29
Q

What is the treatment of choice for…
pyloric stenosis?
Bleeding duodenal ulcer resistant to adrenaline?

A
PS = Gastroenterostomy 
Ulcer = Under-running
30
Q

What are duodenal ulcers relieved by eating?

A

Release of alkaline juices from the pancreas

31
Q
What artery does each branch off from...
Right gastroepiploic artery?
Left gastroepiploic?
Right gastric?
Left gastric?
A

Gastroduodenal artery
Splenic
Proper hepatic
Celiac trunk

32
Q

What are the layers of the anterior abdominal wall?

A

Skin - superficial fascia - rectus sheath - rectus abdominis - external oblique - internal oblique - transverse abdominis - transverse fascia - extraperitoneal tissue - peritoneum

33
Q

What does SAD PUCKER stand for?

A
Suprarenal glands
Aorta and IVC
Duodenum
Pancreas
Ureters
Colon (descending and ascending)
Kidneys
Esophagus
Rectum
34
Q

What are the 3 types of achalasia?
Which is the most common?
What has the worst treatment response?

A

Type 1 - achalasia with minimal oesophageal pressurisation
Type 2 - achalasia with oesophageal compression (most common)
Type 3 - achalasia with spasm (worst treatment response)

35
Q

What sort of cells line the mucosa of the oesophagus?

What are the 3 layers in the mucosa?

A

Stratified squamous epithelium

Mucous epithelium, lamina propria and muscularis mucosae

36
Q

5 different options for antiemetics.
What does each do?
Which are contraindicated in prolonged QTc syndrome?

A

Metoclopramide - Dopamine antagonist, increases gastric motility and increases LOS tone
Ondansetron - serotonin antagonist CNS and PNS (prolonged QT)
Droperidol - dopamine antagonist in chemoreceptor trigger zone (prolonged QT)
Dexamethasone - unknown
Prochlorperazine - dopamine antagonist