GASTRO Flashcards
what is GORD?
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.
what are the risk factors for GORD?
- fam history
- older age
- hiatus hernia
- obesity
what is dispepsia?
a non-specific term used to describe indigestion
what are the symptoms of GORD?
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
when should a patient with symptoms of GORD be referred for endoscopy?
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
how is GORD managed?
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)
what effect does H.pylori have on the stomach?
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.
why do people need to have H.pylori test before offering PPI?
Because PPI will effect the result of H.pylori test.
what tests can be used for H.pylori?
urea breath test
stool antigen test
rapid urease test
how is a H.pylori test treated?
the eradication involves triple therapy with a proton pump inhibitor, plus 2 antibiotics (e.g. metronidazole and clarithromycin or amoxicillin and clarithromycin)
what is barrettes oesophagus?
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.
what is a Mallory-Weiss tear?
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 .
what are the risk factors for hematemesis?
condition predisposing to retching, vomiting and/or straining chronic cough hiatal hernia retching during endoscopy significant alcohol use
what investigations should you perform for suspected mallory Weiss tear?
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
what are some causes of upper GI bleed?
oesophageal varicies
Mallory-Weiss tear (tear of the oesophageal mucous membrane
ulcers of the stomach or duodenum
cancers of the stomach or duodenum
what scoring system is used to assess the risk of an upper GI bleed?
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.
why does urea rise in upper GI bleed?
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
what is the Rockall score?
the Rocakall score is used for patients that have had an endoscopy to calculate the risk of re-bleeding and overall mortality.
how do you manage and upper GI bleed?
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
what is a group and save?
what is a crossmatch ?
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.
what causes stomach ulceration?
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
how does a peptic ulcer present?
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
what investigations would you perform for peptic ulcer?
h pylori urea breath test or stool antigen test
upper GU endoscopy
FBC
how do you manage peptic ulcers?
PPI
what are the complications of peptic ulcer?
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
what is achalasia?
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
what are the clinical features of achalasia?
dysphagia of both solids and liquids
typically variation in severity of symptoms
heartburn
regurgitation of food - may lead to cough, aspiration pneumonia
what investigations would you perform for achalasia?
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
how do you manage achalasia?
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
what is the most common cause of gastritis?
and what are other causes?
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
how does gastritis present?
epigastric pain
vomiting
haematemesis
how do you manage gastritis?
give PPI or ranitidine
eradicate H.pylori
what are the symptoms of malabsorption?
diarrhoea weight loss lethargy steatorrhoea bloating
what is coeliac disease?
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
what antibodies are involved in coeliac disease?
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
what part of the bowel does coeliac disease effect?
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
how does coeliac disease present?
it can be asymptomatic FTT in young children diarrhoea fatigue weight loss mouth ulcers anaemia secondary to iron, B12 or folate deficiency dermatitis herpetiformis
what investigations would you perform for coeliac disease?
***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
which conditions does nice guidelines recommend screening for coeliac disease?
- autoimmune thyroid disease
- dermatitis herpetiformis
- IBS
- Type 1 diabetes
- first degree relative with coeliac disease
what are the complications of untreated coeliac disease?
vitamin deficiency anaemia osteoporosis ulcerative jejunitis enteropathy associated T-cell lymphoma of the intestine non-hodgkins lymphoma small bowel adenocarcinome
how is coeliac disease managed?
life long gluten free diet
calcium, vitamin D and iron supplementation may be given
what is tropical sprue?
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
what is ulcerative colitis?
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.
what are the peak incidence for UC?
15-25 years
55-65 years
what are the symptoms of UC?
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the lower left quadrant
weight loss
extra-intestinal features - arthritis, erythema nodosum, episcleritis, osteoporosis
what are the genetic assosiations with coeliac disease?
HLA DQ2 gene
HLA DQ8 gene
what investigations would you perform for ulcerative colitis?
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
what would colonoscopy and biopsy show in UC?
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
what would a barium enema show in UC?
loss of haustrations
superficial ulceration - pseudopolyps
in long standing disease there will be a ‘drainpipe colon’
how is UC managed?
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
what are the complications of UC?
toxic megacolon - fulminant or sever colitis perforation masive lower GI bleed colonic adenocarcinoma benign stricture inflammatory pseudopolyps primary sclerosing sholangitis
what is crohns disease?
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.
what are the symptoms of Crohn’s disease ?
- 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
what investigations would you perform for Crohn’s disease?
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
how do you manage Crohn’s?
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
what are the things that make you think it is crohn’s and not UC?
blood/mucus less common affects entire GI tract Skip lesions on endoscopy Terminal ileum most effected transmural inflammation smoking is risk factor
what are the complications of Crohn’s disease ?
intestinal obstruction intra abdominal sepsis sinuses toxic megacolon anaemia short bowel syndrome malignancy kidney stones
what do you need to assess before offering azathioprine or mercaptopurine?
asses thiopurine methyltransferase (TPMT)
how is the severity of UC classified?
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
what are some extra-intestinal manifestations of IBD?
uveitis episcleitis conjunctivitis arthralgia arthritis erythema nodosum pyoderma gangrenosum fatty liver sclerosing cholangitis oxylate stones in patients with small bowel disease
what are the different types of intestinal obstruction
functional and mechanical
what are the causes of small bowel obsrtuction?
adhesions hernias crohn's disease intussusceptions obstruction due to intrinsic involvement by cancer
what are some causes of colonic obstruction?
carcinoma of the colon
sigmoid volvulus
diverticular disease
what can cause functional bowel obstruction?
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.
what are the symptoms of small bowel obstruction?
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
what investigations would you perform for small bowel obstruction?
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
how do you manage a small bowel obstruction ?
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
what are the complications of small bowel obstruction ?
intestinal necrosis sepsis multi-organ failure intra-abdominal abscess intestinal perforation
what are the symptoms of a large bowel obstruction?
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
what investigations would you perform for large bowel obstruction ?
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
how is large bowel obstruction managed?
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
complications of large bowel obstruction ?
perforation
sepsis
death
what is an intussusception?
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
what are the features of intussusception?
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
what would an USS show in intussusception?
target like mass
how is intussusception managed?
majority treated with reduction by air insufflation under radiological controlled
if this fails - surgery
what is a volvulus?
a twisting of the GI tract which leads to partial or complete bowel obstruction
what are the sites of volvulus?
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)
how is volvulus diagnosed?
abdo x ray - coffee bean sign if sigmoid volvulus
CT scan
what are the symptoms of volvulus?
constipation
abdominal bloating
abdominal pain
nausea and vomiting
how do you manage volvulus ?
sigmoid - endoscopic decompression - rigid sigmoidoscopy with rectal tube insertion
caecal volvulus - management is usually operative
surgical management
hartmann’s procedure (sigmoid)
right hemicolectomy (caecal)
what is a pseudo bowel obstruction
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
what parts of the bowel does a pseudo-obstruction usually effect?
the caecum and the ascending colon
however can affect the bowel
what are some causes of pseudo-obstruction?
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
what are the clinical features of a pseudo-obstruction?
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
what investigations would you perform for pseudo-obstruction?
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
how do you manage pseudo bowel obstruction ?
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
what can cause oesophageal motility disorder?
achalasia
diffuse oesophageal spasm
autoimmune and connective tissue disorders - systemic sclerosis, polymyositis and dermatomyositits
what is diffuse oesophageal spasm?
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
what are the symptoms of diffuse oesophageal spasm?
severe dysphagia
central chest pain exacerbated by food
it can respond to nitrates - making it difficult to distinguish from angina.
what investigations would you perform for diffuse oesophageal spasm?
manometry - shows a pattern of repetitive, simultaneous and ineffective contractions of the oesophagus
how do you manage diffuse oesophageal spasm
nitrates
CCB
pneumatic dilatation
