GASTRO Flashcards

1
Q

what is GORD?

A

where acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus
The oesophagus has a squamous epithelial lining making it more sensitive to the effects of stomach where as the stomach has columnar epithelial lining that is more protected against stomach acid.

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2
Q

what are the risk factors for GORD?

A
  • fam history
  • older age
  • hiatus hernia
  • obesity
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3
Q

what is dispepsia?

A

a non-specific term used to describe indigestion

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4
Q

what are the symptoms of GORD?

A
heartburn 
acid regurgitation 
retrosternal or epigastric pain 
bloating 
globus (patients may describe a lump in the throat that is present despite swallowing) 
nocturnal cough
hoarse voice
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5
Q

when should a patient with symptoms of GORD be referred for endoscopy?

A

patients with evidence of a GI bleed need admission and urgent endoscopy
patients with symptoms suspicious of cancer should have a two week wait referral so that endoscopy is performed within two weeks
they key red flag features indicating referral are:
- dysphagia (difficulty swallowing)
- aged over 55
- weight loss
- upper abdo pain/reflux
- treatment resistant dyspepsia
- nausea and vomiting
- low Hb
- raised platelet count

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6
Q

how is GORD managed?

A

Lifestyle advice

  • reduce tea, coffee and alcohol
  • weight loss
  • avoid smoking
  • smaller lighter meals
  • avoid heavy meals before bed time
  • stay upright after meals rather than lying flat

Patients can take acid neutralising medication when requires - Gaviscon, Rennie

PPI - omeprazole, lansoprazole

Ranitidine (H2 receptor antagonist - antihistamine)

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7
Q

what effect does H.pylori have on the stomach?

A

it is a gram negative bacteria that lives in the stomach and causes damage to the epithelial lining of the stomach resulting in gastritis, ulcers and increasing risk of stomach cancer.
It produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells.

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8
Q

why do people need to have H.pylori test before offering PPI?

A

Because PPI will effect the result of H.pylori test.

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9
Q

what tests can be used for H.pylori?

A

urea breath test
stool antigen test
rapid urease test

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10
Q

how is a H.pylori test treated?

A

the eradication involves triple therapy with a proton pump inhibitor, plus 2 antibiotics (e.g. metronidazole and clarithromycin or amoxicillin and clarithromycin)

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11
Q

what is barrettes oesophagus?

A

constant reflux of acid results in the lower oesophageal epithelium changing in a process know as metaplasia from squamous to columnar epithelium. This change is called barretts oesophagus.

other risk factors - male, smoking, central obesity

it is pre-malignant condition and is a risk factor for the development of adenocarcinoma of the oesophagus.

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12
Q

what is a Mallory-Weiss tear?

A

it is characterised by a tear or laceration often along the right border of, or near the gastro-oesophageal junction
commonly presents with haematemesis after an episode of forceful or recurrent retching, vomiting, coughing or straining .

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13
Q

what are the risk factors for hematemesis?

A
condition predisposing to retching, vomiting and/or straining 
chronic cough 
hiatal hernia 
retching during endoscopy 
significant alcohol use
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14
Q

what investigations should you perform for suspected mallory Weiss tear?

A

FBC - incase they need blood transfusion
Urea - important parameter to evaluate the severity of the bleeding - will be high in a patient with ongoing bleeding
LFTs - rule out liver disease which may predispose to varicies
INR
oesophagogastroduodenoscopy

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15
Q

what are some causes of upper GI bleed?

A

oesophageal varicies
Mallory-Weiss tear (tear of the oesophageal mucous membrane
ulcers of the stomach or duodenum
cancers of the stomach or duodenum

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16
Q

what scoring system is used to assess the risk of an upper GI bleed?

A

Glasgow-Blatchford score - used in suspected upper GI bleed on their initial presentation to help you to decide a plan and weather to discharge or not.

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17
Q

why does urea rise in upper GI bleed?

A

because they blood in the GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is the urea and this urea is then absorbed in the intestines

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18
Q

what is the Rockall score?

A

the Rocakall score is used for patients that have had an endoscopy to calculate the risk of re-bleeding and overall mortality.

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19
Q

how do you manage and upper GI bleed?

A

ABCDE approach to immediate resuscitation
bloods (FBC, U&E’s, INR, LFTs, cross match 2 units of blood)
get two large bore cannulas in
transfusion
endoscopy
stop anticoagulants and NSAIDS

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20
Q

what is a group and save?

what is a crossmatch ?

A

group and save is where the lab simply check the patients blood group and keeps a sample of their blood saved incase they need to match blood to it

crossmatch is where the lab actually finds blood, tests that it is compatible and keeps it ready in the fridge to be used if necessary.

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21
Q

what causes stomach ulceration?

A

increase in stomach acid which can be caused by stress, alcohol, caffeine, smoking, spicy foods
breakdown of the protective layer of the stomach and duodenum which can be caused by medications (steroids or NSAIDs) and H.pylori

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22
Q

how does a peptic ulcer present?

A

epigastric discomfort or pain (typically if a gastric ulcer it worsens on eating and if a duodenal ulcer pain improves with eating)
nausea and vomiting
dyspepsia
bleeding causing haematemesis, coffee ground vomiting and melaena
iron deficiency anaemia due to constant bleeding

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23
Q

what investigations would you perform for peptic ulcer?

A

h pylori urea breath test or stool antigen test
upper GU endoscopy
FBC

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24
Q

how do you manage peptic ulcers?

A

PPI

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25
Q

what are the complications of peptic ulcer?

A

bleeding from the ulcer
perforation resulting in an acute abdomen and peritonitis (this requires urgent surgical repair )
scarring and strictures this can lead to pyloric stenosis

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26
Q

what is achalasia?

A

failure of oesophageal peristalsis (failure of contraction of the oesophageal muscle) and failure of relaxation of lower oesophageal sphincter due to degenerative loss of ganglia from Auerbach’s plexus which impairs oesophageal emptying

Achalasia typically presents in middle age and is equally common in men and woman

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27
Q

what are the clinical features of achalasia?

A

dysphagia of both solids and liquids
typically variation in severity of symptoms
heartburn
regurgitation of food - may lead to cough, aspiration pneumonia

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28
Q

what investigations would you perform for achalasia?

A

oesophageal manometry - the manometry will show excessive LOS tone which doesn’t relax on swallowing and absence of oesophageal peristalsis - considered the most important diagnostic test
barium swallow shows grossly expanded oesophagus, fluid level, birds beak appearance
CXR - wide mediastinum, fluid levels
upper gastrointestinal endoscopy

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29
Q

how do you manage achalasia?

A

good surgical candidate - pneumatic balloon dilatation or heller cardiomyotomy

if poor surgical candidate - CCB or nitrates can be partly effective for temporary relief, injection of botulinum A can be used but are only effective for a few months

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30
Q

what is the most common cause of gastritis?

and what are other causes?

A

H.pylori infection is the most common cause

other causes include: autoimmune gastritis, viruses and duodeno-gastric reflux, alcohol, NSAIDs, reflux/hiatus hernia, granulomas (crohn’s, sarcoidosis), CMV

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31
Q

how does gastritis present?

A

epigastric pain
vomiting
haematemesis

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32
Q

how do you manage gastritis?

A

give PPI or ranitidine

eradicate H.pylori

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33
Q

what are the symptoms of malabsorption?

A
diarrhoea 
weight loss 
lethargy 
steatorrhoea 
bloating
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34
Q

what is coeliac disease?

A

an autoimmune condition where exposure to gluten causes and autoimmune reaction in the small bowel - it usually develops in early childhood but can develop t any age

In coeliac auto-antibodies are created in response to exposure to gluten that target the epithelial cells of the intestine and lead to inflammation

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35
Q

what antibodies are involved in coeliac disease?

A

anti-tissue transglutaminase (anti-TTG) -IgA
anti-endomysial (anti-EMA) - IgA
deaminated gliadin peptide antibody (anti DGPs)

these antibodies relate to disease activity and will rise with more active disease and may disappear with effective treatment.

When you test for the antibodies, it is important to test for total immunoglobulin A levels as if they have an IgA deficiency then the coeliac test will be negative

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36
Q

what part of the bowel does coeliac disease effect?

A

inflammation affects the small bowel - particularly the jejunum
it causes atrophy of the intestinal villi which usually help with absorbing nutrients from the food passing through the intestine
the inflammation causes malabsorption of nutrients and the symptoms of the disease

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37
Q

how does coeliac disease present?

A
it can be asymptomatic 
FTT in young children 
diarrhoea 
fatigue 
weight loss 
mouth ulcers 
anaemia secondary to iron, B12 or folate deficiency
dermatitis herpetiformis
38
Q

what investigations would you perform for coeliac disease?

A

***investigations must be carried out whilst the patient remains on a diet containing gluten otherwise it will not be possible to detect the antibodies

check total IgA antibodies to exclude IgA deficiency before checking for coeliac disease
check anti TTG antibodies and anti-EMA antibodies

endoscopy and intestinal biopsy will show crypt hypertrophy and villous atrophy and the presence of intra-epithelial lymphocytes and lamina propria infiltration with lymphocytes

39
Q

which conditions does nice guidelines recommend screening for coeliac disease?

A
  • autoimmune thyroid disease
  • dermatitis herpetiformis
  • IBS
  • Type 1 diabetes
  • first degree relative with coeliac disease
40
Q

what are the complications of untreated coeliac disease?

A
vitamin deficiency 
anaemia 
osteoporosis 
ulcerative jejunitis 
enteropathy associated T-cell  lymphoma of the intestine 
non-hodgkins lymphoma 
small bowel adenocarcinome
41
Q

how is coeliac disease managed?

A

life long gluten free diet

calcium, vitamin D and iron supplementation may be given

42
Q

what is tropical sprue?

A

a disease that causes progressive villous atrophy in the small intestine that is similar to coeliac sprue
it is believed to be initiated or sustained by a still undefined infection
it occurs in residents or visitors to endemic areas in the tropics

small bowel biopsy will show similar things to untreated coeliac

treatment with folic acid and tetracycline for 3-6 months

43
Q

what is ulcerative colitis?

A

it is a form of inflammatory bowel disease - the inflammation starts in the rectum (the most common site for UC) and never spreads past the ileocaecal valve. It is continuous.

44
Q

what are the peak incidence for UC?

A

15-25 years

55-65 years

45
Q

what are the symptoms of UC?

A

bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the lower left quadrant
weight loss
extra-intestinal features - arthritis, erythema nodosum, episcleritis, osteoporosis

46
Q

what are the genetic assosiations with coeliac disease?

A

HLA DQ2 gene

HLA DQ8 gene

47
Q

what investigations would you perform for ulcerative colitis?

A

stool studies - faecal calprotectin is elevated if there is bowel inflammation
FBC
LFTs - should be checked every 6-12 months for surveillance of primary sclerosing cholangitis as it is much more common in UC
ESR and CRP
flexible sigmoidoscopy (findings will be the same as colonoscopy but examination is limited to the distal colon)
colonoscopy plus biopsies
barium enema

48
Q

what would colonoscopy and biopsy show in UC?

A

colonoscopy will show

  • continuous uniform involvement
  • loss of vascular markings
  • diffuse erythema
  • mucosal granularity

biopsies will show

  • inflammatory cells infiltrate in lamina propria
  • neutrophils migrate through the wallas of glands to form crypt abcesses
  • depletion of goblet cells
  • continuous distal disease
  • mucin depletion
  • basal plasmacytosis
  • diffuse mucosal atrophy
  • absence of granulomas
  • anal sparing
  • only the superficial mucosa is affected
49
Q

what would a barium enema show in UC?

A

loss of haustrations
superficial ulceration - pseudopolyps
in long standing disease there will be a ‘drainpipe colon’

50
Q

how is UC managed?

A

Inducing remission

In fulminant disease - admission plus IV corticosteroid (hydrocortisone)

severe non fulminant disease - first line aminosalicylate e.g. mesalazine oral and rectal. Second line - corticosteroid - prednisolone - (this can be added to first line treatment). If this does not work - admission and IV hydrocortisone

mild/moderate disease - 1st line topical mesalazine , 2nd line - topical corticosteroid - hydrocortisone rectal or oral mesalazine)

MANAGING DISEASE IN REMISSION
1st line mesalazine 2nd line oral beclametasone

Refractory disease
1st line - thiopurines (azathioprine)
2nd line - TNF alpha inhibitor (infliximab)

if all else fails - colectomy

51
Q

what are the complications of UC?

A
toxic megacolon - fulminant or sever colitis 
perforation 
masive lower GI bleed 
colonic adenocarcinoma 
benign stricture 
inflammatory pseudopolyps 
primary sclerosing sholangitis
52
Q

what is crohns disease?

A

Crohn’s disease is a form of inflammatory bowel disease.

It commonly affects the terminal ileum and colon but may be seen anywhere from the mouth to the anus.

53
Q

what are the symptoms of Crohn’s disease ?

A
  • it usually presents in late adolescence or early adulthood
  • presentation may be non-specific such as weight loss and lethargy
  • diarrhoea - the most prominent symptom in adults, crohn’s colitis may cause bloody diarrhoea
  • abdo pain - the most prominent symptom in children
  • perianal disease e.g. skin tags or ulcers

other symptoms include - bowel obstruction, blood in stools, fever, fatigue, abdo tenderness

54
Q

what investigations would you perform for Crohn’s disease?

A

Bloods - FBC, iron studies, serum vitamin B12, serum folate, comprehensive metabolic panel , CRP and ESR

stool testing - faecal calprotectin

Endoscopy (OGD and colonoscopy) with biopsy (inflammation in all layers from mucosa to serosa, goblet cells, granulomas, deep ulcer, skip lesion)

small bowel enema - strictures (kantor’s string sign), proximal bowel dilatation, rose thorn ulcers, fistulae

plain abdo x-ray - will show small bowel or colonic dilatation, calcification, sacroilitits, intra-abdominal abscesses
CT/MRO abdo - skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae

55
Q

how do you manage Crohn’s?

A

inducing remission - steroids - budesonide. If this doesn’t work consider adding immunosuppressant (azathioprine, mercaptopurine)

maintaining remission - first line azathioprine, mercaptopurine. Second line - methotrexate, infliximab, adalimumab

surgery

56
Q

what are the things that make you think it is crohn’s and not UC?

A
blood/mucus less common 
affects entire GI tract 
Skip lesions on endoscopy 
Terminal ileum most effected 
transmural inflammation 
smoking is risk factor
57
Q

what are the complications of Crohn’s disease ?

A
intestinal obstruction 
intra abdominal sepsis 
sinuses 
toxic megacolon 
anaemia 
short bowel syndrome 
malignancy 
kidney stones
58
Q

what do you need to assess before offering azathioprine or mercaptopurine?

A

asses thiopurine methyltransferase (TPMT)

59
Q

how is the severity of UC classified?

A

mild - < 4 stools/day, only small amount of blood
moderate - 4-6 stools/day, varying amounts of blood, no systemic upset
severe - >6 stools per day plus features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers) - should be treated in hospital

60
Q

what are some extra-intestinal manifestations of IBD?

A
uveitis 
episcleitis 
conjunctivitis 
arthralgia 
arthritis 
erythema nodosum 
pyoderma gangrenosum 
fatty liver 
sclerosing cholangitis 
oxylate stones in patients with small bowel disease
61
Q

what are the different types of intestinal obstruction

A

functional and mechanical

62
Q

what are the causes of small bowel obsrtuction?

A
adhesions 
hernias 
crohn's disease 
intussusceptions 
obstruction due to intrinsic involvement by cancer
63
Q

what are some causes of colonic obstruction?

A

carcinoma of the colon
sigmoid volvulus
diverticular disease

64
Q

what can cause functional bowel obstruction?

A

occurs with a paralytic ileus - often seen post-operative, stage of peritonitis, or of major abdo surgery or in association with opiate treatment
it also occurs when the nerves or muscles of the intestine are damaged, causing intestinal pseudo-obstruction.

65
Q

what are the symptoms of small bowel obstruction?

A
constipation 
failure to pass stool or flatus 
intermittent abdominal pain describes as cramping, intermittent and sever
vomiting, may be bilious 
abdo distension 
abdo tenderness 
abdo mass 
palpable rectal mass 
peritonitis
66
Q

what investigations would you perform for small bowel obstruction?

A

CT of abdo and pelvis with oral and IV contrast (may visualise transition zone, mass, tumour, appendicitis
abdominal x ray (distended loops of bowel - upper limits of normal are 3cm small bowel, 6cm colon and 9cm caecum)
FBC, U&E, CRP, glucose

67
Q

how do you manage a small bowel obstruction ?

A

Nil by mouth
IV fluids
NG tube on free drainage to allow stomach contents to feely drain and prevent need for vomiting

surgery and correct underlying cause

68
Q

what are the complications of small bowel obstruction ?

A
intestinal necrosis 
sepsis 
multi-organ failure 
intra-abdominal abscess
intestinal perforation
69
Q

what are the symptoms of a large bowel obstruction?

A
colicky abdominal pain 
abdominal distension 
tympanic abdomen 
change to bowel habits 
hard faeces 
empty rectum 
recent weight loss 
rectal bleeding 
abnormal bowel sounds 
palpable abdominal mass
vomiting would occur later than if it was a small bowel obstruction 
absolute constipation would occur earlier with a large bowel obstruction compared to small bowel obstruction 
tinkling bowel sounds
70
Q

what investigations would you perform for large bowel obstruction ?

A

FBC, U&E, Renal function, coagulation studies
erect chest x-ray (look for sub-diaphragmatic free air - suggests perforation)
plain abdo x-ray - gaseous distension of large bowel

also consider contrast enema, CT abdomen and pelvis

71
Q

how is large bowel obstruction managed?

A

supportive measures - IV fluds, oxygen etc
emergency surgery if suspected or impending perforation

sigmoid volvulus - flexible or rigid sigmoidoscopy - can relieve obstruction - if this fails then surgery is needed

ceacal volvulus - surgery

malignancy - surgery

large bowel will usually need surgery

72
Q

complications of large bowel obstruction ?

A

perforation
sepsis
death

73
Q

what is an intussusception?

A

describes the invagination of one portion of the bowel into the lumen of the adjacent bowel - most commonly around the ileo-caecal region

it usually affects infants between 6-18 months boys more commonly affected than girls

74
Q

what are the features of intussusception?

A

paroxysmal abdo colic pain
during the paroxym the infant will characteristically draw their knees up nd turn pale
vomiting
bloodstained stool - red current jelly - late sign
sausage shaped mass in the right upper quadrant

75
Q

what would an USS show in intussusception?

A

target like mass

76
Q

how is intussusception managed?

A

majority treated with reduction by air insufflation under radiological controlled
if this fails - surgery

77
Q

what is a volvulus?

A

a twisting of the GI tract which leads to partial or complete bowel obstruction

78
Q

what are the sites of volvulus?

A
gastric volvulus - twisting of the stomach, rare 
sigmoid volvulus (associated with older patients, chronic constipation, chagas disease, neuro condition (parkinsons, duchenne muscular atrophy), psychiatric conditions (schizophrenia) 
caecal volvulus (small bowel obstruction may be seen) (all ages, adhesions, pregnancy)
79
Q

how is volvulus diagnosed?

A

abdo x ray - coffee bean sign if sigmoid volvulus

CT scan

80
Q

what are the symptoms of volvulus?

A

constipation
abdominal bloating
abdominal pain
nausea and vomiting

81
Q

how do you manage volvulus ?

A

sigmoid - endoscopic decompression - rigid sigmoidoscopy with rectal tube insertion
caecal volvulus - management is usually operative

surgical management
hartmann’s procedure (sigmoid)
right hemicolectomy (caecal)

82
Q

what is a pseudo bowel obstruction

A

pseudo obstruction, also known as ogilive syndrome in the acute setting, is a disorder characterised by dilatation of the colon due to an adynamic bowel in the absence of mechanical obstruction.

rare condition, most commonly seen in the elderly

can lead to a toxic mega colon, bowel ischaemia and perforation

83
Q

what parts of the bowel does a pseudo-obstruction usually effect?

A

the caecum and the ascending colon

however can affect the bowel

84
Q

what are some causes of pseudo-obstruction?

A

electrolyte imbalance or endocrine disorder (hypercalcaemia, hypothyroidism or hypomagnesaemia)

meds - opioids, CCB, antidepressants

recent surgery, severe illness or trauma - including cardiac ischaemia

neurological disease - parkinson’s, MS, hirschsprung’s disease

85
Q

what are the clinical features of a pseudo-obstruction?

A

most patients will present with clinical features of mechanical bowel obstruction

  • abdo pain
  • abdo distension
  • constipation (due to adynamic bowel, whilst not passing normal stool, often patients may have paradoxical diarrhoea)
  • vomiting
86
Q

what investigations would you perform for pseudo-obstruction?

A

blood should be done to assess for biochemical or endocrine causes
plain abdominal x-ray (will show the same as mechanical obstruction)
abdominal-pelvis CT scan with IV contrast - this will help exclude mechanical cause

87
Q

how do you manage pseudo bowel obstruction ?

A

conservative
if they do not resolve, endoscopic decompression will be the mainstay of treatment. If this is limited resolution the the use of IV neostigmine may also be trialled if suitable

surgical management - may require segmental resection or caecostomy or ileostomy

88
Q

what can cause oesophageal motility disorder?

A

achalasia
diffuse oesophageal spasm
autoimmune and connective tissue disorders - systemic sclerosis, polymyositis and dermatomyositits

89
Q

what is diffuse oesophageal spasm?

A

a disease characterised by multi-focal high amplitude contraction of the oesophagus

it is thought to be caused by the dysfunction of the oesophageal inhibitory nerves and it can progress to achalasia

90
Q

what are the symptoms of diffuse oesophageal spasm?

A

severe dysphagia
central chest pain exacerbated by food

it can respond to nitrates - making it difficult to distinguish from angina.

91
Q

what investigations would you perform for diffuse oesophageal spasm?

A

manometry - shows a pattern of repetitive, simultaneous and ineffective contractions of the oesophagus

92
Q

how do you manage diffuse oesophageal spasm

A

nitrates
CCB
pneumatic dilatation