Gastrointestinal Flashcards
at what point does reflux of gastric contents into the oesophagus become GORD, instead of a normal occurrence?
when it begins to cause symptoms
what 3 problems might prolonged GORD cause?
oesophagitis, benign oesophageal strictures, Barrett’s oesophagus
give 3 causes of GORD
lower oesophageal sphicter hypotension, hiatus hernia, loss of oesophageal peristaltic function, abdominal obesity, gastric acid hypersecretion, slow gastric emptying
give 3 risk factors for GORD
overeating, smoking, alcohol, pregnancy, surgery in achalasia, drugs, systemic sclerosis
explain the pathophysiology of GORD
LOS tone reduced + frequent transient LOS relaxation.
increased mucosal sensitivity to gastric acid + reduced oesophageal clearance of acid.
describe the pain felt in GORD
burning pain, aggravated by lying flat/bending over and on drinking hot drinks/alcohol, after big meals - relieved by antacids.
give 2 features of GORD, apart from chest pain
belching, acid/bile regurgitation, increased saliva production, odynophage (painful swallowing)
give 2 extra-oesophageal features of GORD
nocturnal asthma, chronic cough, laryngitis (hoarseness, throat clearing), sinusitis
give 2 possible complications of GORD
oesophagitis, ulcers, benign stricture, iron-deficiency. Barrett’s oesophagus.
what is Barrett’s oesophagus? how does it put GORD patients at greater risk of oesophageal cancer?
distal oesophageal epithelium undergoes metaplasia from squamous to columnar.
metalplasia -> dyplasia -> neoplasia.
this pattern means those with low-grade Barrett’s oesophagus are more likely to progress to cancer.
give 3 differential diagnoses of GORD
oesophagitis due to corrosives, NSAIDs, herpes, Candida.
duodenal/gastric ulcers or cancers.
non-ulcer dyspepsia.
sphincter of Oddi malfunction.
cardiac disease.
give 3 red flag features of upper GI diseases. what would you do if a patient had these?
ALARM symptoms:
Anaemia (iron-deficiency)
Loss of weight.
Anorexia.
Recent onset/progressive symptoms.
Malaena/haematemesis.
Swallowing difficulty.
endoscopy to check for upper GI cancers.
describe the lifestyle changes you would advise a GORD patient to make
lose weight, avoid alcohol, hot drinks, citrus fruits, fizzy drinks, spicy foods etc.
smoking cessation.
raise bed head.
eat small regular meals, don’t eat close to bed time.
how might you manage GORD, beyond lifestyle changes?
antacids or alginates.
oesophagitis - PPIs (lansoprazole, omeprazole etc).
H2-receptor blockers (rantidine).
laprascopic surgery - increase LOS pressure.
how do alginates/antacids work?
usually given as compound preparations.
antacids buffer stomach acid.
alginates increase the viscosity of stomach contents.
they form a floating ‘raft’ separating gastric contents from the gastro-oesophageal junction.
how do PPIs work?
irreversibly inhibit gastric H+/K+-ATPase.
block luminal secretion of gastric acid.
by targeting this final stage of gastric acid production, they can suppress it almost completely - more effective than H2 receptor blockers.
how do H2 receptor antagonists work?
reduce gastric acid secretion. they block the H2 (histamine) receptors on the gastric parietal cell, preventing activation of the proton pump.
pump still stimulated by other pathways, so H2 receptor blockers are not as effective as PPIs.
what causes a Mallory-Weiss tear? how might it present
persistent vomiting/retching - causes haematemesis via an oesophageal mucosal tear.
what are Mallory-Weiss tears associated with?
alcoholism and eating disorders
what is a peptic ulcer? where do they usually occur?
an ulcer of the mucosa in/adjacent to an acid-bearing area.
stomach + proximal duodenum. - duodenum more common.
what two things cause most peptic ulcers?
H. pylori
NSAIDs/aspirin
list 3 risk factors for duodenal ulcers
- H pylori
- NSAIDs, steroids, SSRIs
increased gastric acid secretion.
increased gastric emptying (lowers duodenal pH).
blood group O.
smoking.
list 3 risk factors for gastric ulcers
H pylori, smoking, NSAIDs, reflux of duodenal contents, delayed gastric emptying
what are the differences between the epigastric pain of a gastric ulcer and of a duodenal ulcer?
gastric - worse with food, better when hungry.
duodenal - worse when hungry, better with food or milk.
give 2 features of peptic ulcer disease apart from epigastric pain
bloating, fullness after meals, heartburn, tender epigastrium.
what investigations would be carried out in peptic ulcer disease? what would you expect to see?
endoscopy - biopsy all ulcers to exclude malignancy.
C13-urea breath test for H pylori ± stool antigen test - immunoassay using monoclonal antibodies.
how would you treat an H pylori +ve peptic ulcer patient?
eradication regimens - omeprazole + metronidazole + clarithromycin.
how would you treat an H pylori -ve peptic ulcer patient?
stop aspirin/NSAIDs.
PPIs - lansoprazole (or rantidine - H2 blocker).
give 2 possible complications of peptic ulcer disease
perforation (surgical closure, drain abdo).
bleeding.
malignancy.
gastric outflow obstruction.
what group of patients is at highest risk of developing oesophageal varices? why?
cirrhosis patients - portal hypertension causes dilated collateral veins at site of portosystemic anastomoses
what is the complication risk with oesophageal varices?
that they will cause an acute haemorrhage - life-threatening.
the varices protrude into oesophageal lumen so are easily traumatised by passing food.
how would you manage a patient bleeding from oesophageal varices?
restore blood volume and correct clotting abnormalities - vit K.
endoscopic banding, sclerosing or cauterising.
vasocontrictors - terlipressin.
give 3 clinical features of achalasia
dysphagia for both solids and liquids.
regurgitation of food, esp at night.
chest pain due to oesophageal spasm.
weight loss.
what is achalasia?
oesophageal motility disorder - LOS fails to relax due to degeneration of the myenteric plexus.
explain the pathogenesis of achalasia
inflammation of myenteric plexus of the oesophagus with ganglion loss - causes loss of nitric oxide, so impaired relaxation of the LOS and oesophageal peristalsis
what might you find on barium swallow of a patient with achalasia?
lack of peristalsis and swan neck/beak deformity at lower oesophagus
what cosmetic drug might help a patient with achalasia?
botulinum toxin A (botox) - injected into LOS
what surgical treatments are available to treat achalasia?
endoscopic balloon dilation or Heller’s cardiomyotomy (surgical division of LOS)
what is the most common cause of gastritis?
H pylori
how do NSAIDs cause gastritis?
they inhibit the COX pathway - COX1 is involved in mucus production so there is a depletion of mucosal prostaglandins
explain the pathology of autoimmune gastritis
combination of atrophic gastritis and loss of parietal cells, which affects the fundus and body of the stomach. there are serum antibodies to gastric parietal cells, which can lead to pernicious anaemia.
what is gastritis?
inflammation of the gastric mucosa - histological diagnosis, usually an incidental finding on gastric mucosal biopsy
list 3 causes of gastritis
H pylori, NSAIDs, autoimmune, viruses, hiatus hernia, alcohol
how might gastritis present?
asymptomatic, or epigastric pain, vomiting, haematemesis
how would you treat gastritis?
ranitidine (H2 blocker) or PPI.
H pylori eradication if needed.
give 3 causes of malabsorption that are common in the UK
coeliac disease, chronic pancreatitis, crohn’s disease
give 3 rarer causes of malabsoprtion
decreased bile - primary biliary cirrhosis, ileal resection, biliary obstruction.
pancreatic insufficiency - pancreatic cancer, cystic fibrosis.
small bowel mucosa - Whipple’s disease, tropical sprue, small bowel resection.
infection - giardiasis, strongloidiasis.
what 3 signs would be seen on histology in coeliac disease?
crypt hyperplasia and villous atrophy + lymphocytic infiltration
what is coeliac disease?
gluten-sensitive enteropathy. T cell mediated autoimmune disease.
abnormal jejunal mucosa that improves when gluten is removed and relapses when gluten is reintroduced.
explain the pathogenesis of coeliac disease
HLA-DQ2/DQ8.
alpha gliadin passes through damaged epithelium of small intestine - deaminated by tissue transglutaminase.
interacts with APCs to activate T cells.
inflammation - leads to villous atrophy and crypt hyperplasia.
give 5 clinical features of coeliac disease
stinking, pale stools that are hard to flush (steatorrhoea).
diarrhoea, abdo pain, bloating, nausea/vomiting, aphthous ulcers, angular stomatitis, weight loss, fatigue, weakness, osteomalacia, failure to thrive.
list 3 differential diagnoses of coeliac disease
IBS, lactose/other food intolerances, IBDs, dermatitis herpetiformis, tropical sprue, bacterial overgrowth, intestinal resection, Whipple’s disease, radiation enteritis.
what 2 signs would you see on serology of a patient with coeliac disease?
low folate/iron, IgA anti-tissue transglutaminase antibodies, anti-enodmyseal antibodies (anti-EMA)
what is the gold standard investigation for coeliac disease?
small bowel biopsy by endoscopy
why would coeliac disease patients be advised to get regular vaccinations?
hyposplenism is common, making them more susceptible to infections
how would you manage coeliac disease?
life-long gluten free diet (must reintroduce gluten a couple of weeks before biopsies taken, but can be stopped initially as a way of identifying coeliac disease).
avoid - wheat, rye and barley.
gluten-free biscuits, flour, bread and pasta are prescribable.
give 2 possible complications of coeliac disease
anaemia, secondary lactose intolerance, increased risk of malignancy, osteoporosis
what is tropical sprue?
a progressive small intestinal disorder occurring in residents/visitors to endemic areas in tropics
describe the pathological features of tropical sprue
villous atrophy + malabsorption (esp. fat and vit B12)
how does tropical sprue present?
diarrhoea, steatorrhoea, megaloblastic anaemia
how would you treat tropical sprue?
tetracycline + folic acid and mineral supplements.
exclude coeliac disease and acute infective diarrhoea.
where in the GI tract might Crohn’s disease affect?
mouth to anus.
describe the lesions seen in Crohn’s disease
skip lesions - there are areas of unaffected bowel between areas of active disease.
there’s transmural inflammation (inflammation spanning full depth of wall) - causes ulceration of superficial mucosa, possibly granulomas
what would you see on endoscopy in Crohn’s disease?
cobblestone appearance - due to skip lesions of inflammation/ulceration and deep fissures.
give 3 symptoms of Crohn’s disease
diarrhoea/urgency.
abdo pain.
weight loss.
fever, malaise, anorexia.
give 3 signs of Crohn’s disease
aphthous ulcers (in mouth).
abdo tenderness/mass.
perianal abscess/fistulas/anal strictures.
extra-GI - clubbing, conjunctivitis, peripheral arthropathies, erythema nodosum, fatty liver, renal stones.
list 3 possible complications of Crohn’s disease
small bowel obstruction, toxic megacolon, abscess formation, fistulae, perforation, colon cancer, fatty liver, PSC, renal stones, osteomalacia, malnutrition, amyloidosis
list 3 differential diagnoses of Crohn’s
UC.
TB, carcinoid syndrome, amyloidosis, infective diarrhoea, bowel carcinoma, ischaemic colitis, diverticulitis, coeliac disease, IBS
what investigation would you carry out to confirm a diagnosis of Crohn’s disease?
endoscopy/colonoscopy with multiple biopsies for histology
how would you manage Crohn’s?
oral steroids - prednisolone, hyrdocortisone.
control diarrhoea with loperamide.
describe the surgical management of Crohn’s disease
not curative, but most will require surgery at some point.
e.g. temporary ileostomy, resection of part of bowel.
NOT bypass and pouch surgery, as too great a risk of recurrence to be worth doing.
what areas of the GI tract may be affected by ulcerative colitis?
just rectum = proctitis.
extended to part of colon = left-sided colitis.
extended to entire colon = pancolitis.
what is the impact of smoking on UC and Crohn’s, respectively?
UC - smoking is protective! incidence is higher in non-smokers.
Crohn’s - smoking doubles risk, and can precipitate relapses.
describe the macro- and microscopic appearances of UC
macro - affects only colon, beginning in rectum and extending proximally. continuous involvement.
red mucosa, easy bleeding.
micro - mucosal inflammation (not full depth/transmural), no granulomata, goblet cell depletion, crypt abscesses.
describe the symptoms of UC
episodic/chronic diarrhoea ± blood and mucus in stool.
crampy abdo discomfort.
bowel frequency relates to severity.
urgency/tenesmus => rectal UC.
give 3 features of an acute, severe attack of UC
fever, malaise, anorexia, weight loss, tachycardia, tender distended abdomen
give 3 extraintestinal signs of UC
clubbing, aphthous oral ulcers, erythema nodosum, episcleritis, conjunctivitis, iritis, large joint arthritis, ankylosing spondylitis, fatty liver, PSC, nutritional deficits, amyloidosis
what investigations would you carry out in UC? what would they show?
colonoscopy - shows disease extent, allows biopsy for histo.
bloods - iron deficiency anaemia, low albumin, possible ANCA +ve.
stool MC&S to exclude infective causes.
how would you treat UC?
mesalazine (a 5-ASA) + prednisolone.
20% will need surgery e.g. coleostomy with ilio-anal pouch.
what are the 5Fs of abdominal distension?
Flatulence, Fat, Foetus, Fluid, Faeces
list 3 causes of small/large bowel obstruction
small bowel - adhesions, hernias.
large bowel - colon carcinoma, constipation, diverticular stricture, volvulus.
describe the clinical features you might see with a higher and lower intestinal obstruction
higher - vomiting, nausea, can still be passing bowel movements.
lower - no passage of faeces or flatulence
what can be heard on examination in both large and small bowel obstruction?
tinkling bowel sounds
how might you manage large/small bowel mechanical obstruction?
small may settle with conservative management - nasogastric suction, IV fluids.
large = surgery.
give 3 causes of mechanical bowel obstruction
adhesions, hernias, Crohn’s disease, intussusception, obstruction due to extrinsic tumour, carcinoma of colon, sigmoid volvulus, diverticular disease
how would mechanical bowel obstruction appear on abdo XR? and in functional obstruction?
mechanical - bowel is dilated above the level of obstruction.
functional - gas seen throughout bowel
give 3 causes of functional bowel obstruction
paralytic ileus, pseudo-obstruction, post-surgery, peritonitis
how would a functional bowel obstruction present differently from a mechanical obstruction?
no pain (although peritonitis pain may be present if this is cause).
decreased bowel sounds.
what is paralytic ileus?
adynamic bowel due to absence of normal peristaltic contractions
give 3 possible causes of paralytic ileus
surgery, pancreatitis/peritonitis, spinal injury, hypokalaemia, hypnoatraemia, uraemia, peritoneal sepsis, tricyclic antidepressants
what is pseudo-obstruction?
appears to be mechanical obstruction, but no cause is found
which part of the bowel does mesenteric ischaemia involve and which vessel is occluded?
small bowel, superior mesenteric artery
give 3 causes of mesenteric ischaemia
superior mesenteric artery thrombosis/embolism, non-occlusive disease, trauma, vasculitis, radiotherapy, strangulation
how does mesenteric ischaemia present?
acute severe abdominal pain, no abdominal signs, rapid hypovolaemia leading to shock.
describe the pain of mesenteric ischaemia
constant, central or around the RIF
what is the main complication you would be worried about in a patient with mesenteric ischaemia?
septic peritonitis - possible progression of SIRS to multi-organ dysfunction syndrome
what antibiotics would you give to a patient with mesenteric ischaemia?
gentamicin + metronidazole
how would you treat mesenteric ischaemia?
Bowel rest (NG tube/NBM)
IV fluids
IV Abx
IV heparin
Prompt laparotomy
Definitive:
Endovascular revascularisation (embolectomy, angioplasty)
Laparotomy
Resection of dead bowel
what vessel is blocked in ischaemic colitis?
inferior mesenteric artery
how might a patient with ischaemic colitis present?
sudden onset abdominal pain and passing of bright red blood ± diarrhoea
what characteristic feature would you see on abdo XR in a patient with ischaemic colitis?
‘thumb printing’ of splenic flexure
what is the gold standard diagnostic investigation in ischaemic colitis?
colonoscopy + biopsy
how would you treat ischaemic colitis?
fluid replacement + abx - most recover, left with strictures
give 2 risk factors of ischaemic colitis
vasculitis, the Pill, thrombophilia, underlying CV disease
name 2 secondary causes of pruritus ani
threadworm infestation, perianal eczema, fungal infection
what are haemorrhoids?
disrupted and dilated anal cushions - there are 3 anal cushions, positioned where the 3 major arteries feeding the vascular plexuses enter the canal.
in what location are haemorrhoids not painful and why?
internal/above the dentate line - lack of nerve supply, can only feel stretch.
give 1 possible cause of haemorrhoids
constipation with prolonged straining.
congestion from pelvic tumour, pregnancy, CCF, portal hypertension
what kind of bleeding would a patient with haemorrhoids experience?
bright red rectal bleeding - coating stools/on tissue/dripping into pan after defectaion
give 2 possible features of haemorrhoids apart from bleeding?
what features would prompt you to consider other pathology?
haemorrhoids - mucous discharge, pruritus ani, severe anaemia.
other - weight loss, tenesmus, change in bowel habit
give 2 differential diagnoses of haemorrhoids
perianal haematoma, anal fissure, abscess, tumour, proctalgia fugax
what investigations should be performed on patients with suspected haemorrhoids?
abdo exam.
PR exam - prolapsing haemorrhoids are obvious, internal haemorrhoids aren’t palpable.
proctoscopy for internal haemorrhoids.
sigmoidoscopy.
describe the management options for haemorrhoids
topical analgesics + stool softener.
rubber band ligation.
sclerosants - phenol injected into the pile.
infra-red coagulation.
surgical - excision haemorrhoidectomy, stapled haemorrhoidopexy.
how do anal fistulae form?
track communicates between skin and anal canal/rectum.
deep intramuscular gland ducts are blocked - abscess form - discharge to form fistula.
give 2 causes of anal fistulae
perianal sepsis, abscesses, Crohn’s disease, TB, diverticular disease, rectal carcinoma
how would you treat an anal fistula?
fistulotomy + excision
what are anal fissures?
painful tear in squamous lining of the lower anal canal
give 2 causes of anal fissures
hard faeces.
parturition.
also - syphilis, herpes, trauma, Crohn’s, anal cancer, psoriasis
how would you treat anal fissures?
local anaesthetic ointments (lidocaine/GTN) or topical diltiazem + stool softeners.
2nd line - botulinum toxin injection.
where are perianal and pilonidal abscesses found in relation to the anus?
perianal - adjacent to anus.
pilonidal - 6cm above the anus.
what is the cause of pilonidal abscesses?
obstruction of natal cleft hair follicles with ingrowing hair
list some diseases that perianal abscess could be the first feature of
Crohn’s, UC, TB
what are the 3 types of IBS?
IBS-C (constipation), IBS-D (diarrhoea), IBS-M (mixed).
give 3 non-intestinal symptoms of IBS
painful periods, premenstrual tension, increased urination, nocturia, back pain, headaches, bad breath, poor sleeping, fatigue, anxiety, depression
what are the diagnostic criteria for IBS?
abdo pain/discomfort must be relieved by defecation or associated with a change in stool form/bowel frequency.
AND 2 of:
urgency, incomplete evacuation, abdominal bloating distension, mucous PR, worsening of symptoms after food
give 2 differential diagnoses of IBS
colonic cancer, IBD (crohn’s/UC), coeliac disease, gastroenteritis, diverticular disease.
what is faecal calprotectin, and when would you test for it?
a marker of bowel inflammation - test for it in diarrhoea, to differentiate between IBD and IBS - faecal calprotecin will be raised in IBD as it is an inflammatory disease.
what investigations should a patient with suspected IBS be given and what would they show?
FBC, ESR, CRP, faecal calprotectin and coeliac antibody screen (for EMA and TTG).
how would you manage IBS?
diet - avoid fibre, fructose, wheat, starch, caffeine, alcohol etc.
constipation = biscodyl and sodium picosulphate (laxatives).
diarrhoea - bulking agent ± loperamide after each loose stool.
colic/bloating - antispasmodics - mebervine, simeticone etc
what is a diverticulum? define diverticulosis and diverticulitis.
diverticulum = outpouching of the gut wall.
diverticulosis = presence of diverticula.
diverticulitis = inflammation of diverticula (usually when faeces obstruct the neck of the diverticulum)
what causes diverticula to form?
thickened muscle layer and high intraluminal pressure (constipation) which forces pouches of mucosa to herniate through the muscular wall at weak points
how are diverticula generally diagnosed?
usually asymptomatic, so commonly an incidental finding at colonoscopy.
what is the best investigation to confirm acute diverticulitis?
CT
how would diverticulitis present?
L iliac fossa pain, fever, nausea, raised WCC, raised CRP/ESR.
tender colon ± localised/generalised peritonitis.
name 2 possible complications of diverticulitis
perforation, abscess formation, peritonitis, formation of fistulas into bladder/vagina, intestinal obstruction.
how would you treat diverticulitis?
analgesia, nil by mouth, IV fluid, abx, CT-guided percutaneous drainage if abscess develops.
name 2 things that may obstruct the lumen of the appendix, allowing gut organisms to invade the appendix wall and leading to appendicitis?
lymphoid hyperplasia, faecolith, filarial worms.
what is the classical feature of appendicitis?
periumbilical pain that moves to right iliac fossa
give 3 signs of appendicitis
tachycardia, fever, furred tongue, lying still, coughing hurts, shallow breaths, guarding of RIF, rebound + percussion tenderness in RIF.
what are the 3 painful signs you would examine for in appendicitis?
Rovsing’s sign - pain greater in RIF than LIF when LIF pressed.
Psoas sign - pain on extending hip.
Cope sign - pain on flexion and internal rotation of right hip.
what are 3 differential diagnoses of appendicitis?
Gynae problems - ruptured ectopic etc - do pregnancy test!
Inflamed Meckel’s diverticulum.
functional bowel disease (IBD, IBS)
describe the management of appendicitis
metronidazole and cefuroxime.
prompt appendicectomy.
what patient groups are at greater risk of primary peritonitis?
liver disease - spontaneous bacterial peritonitis (SBP).
females, immunocompromised, peritoneal dialysis, ascites.
give 3 examples of causes of secondary peritonitis
perforation of hollow viscus, inflammation of abdo organs, peritoneal dialysis, TB, ischaemia of a hollow viscus, chemical.
give 3 symptoms of peritonitis
pain, tendenderness, nausea, chills, rigor, dizziness, weakness and inability to move due to pain
give 3 signs you might find on examination of a peritonitis patient
pyrexia, tachycardia, confusion, guarding, rebound, rigidity, silent abdomen, patient lies very still
what investigations would you perform on a patient with peritonitis?
CXR - look for free air under the diaphragm.
US/CT
how would you manage peritonitis?
ABCs, NG tube, IV fluids, treat underlying cause and treat early- broad spec abx (cephalosporin 3rd gen) following SBP prophylactic oral rifaximin. Surgery for secondary peritonitis: laparotomy- full explosion and lovage (clean) of peritoneum.
what is volvulus?
bowel obstruction due to a loop of bowel that has twisted around the site of its mesenteric attachment
what might be seen on abdominal X ray in a patient with sigmoid volvulus?
‘inverted U’ loop - coffee bean
how would you treat a sigmoid volvulus?
sigmoidoscopy, insertion of a flatus tube.
what might be found on examination of a patient with sigmoid volvulus?
distension of abdomen, increased ‘tinkling’ bowel sounds, tenderness (suggests ischaemia).
describe what occurs in a sliding hiatus hernia
gastro-oesophageal junction slides up into the chest.
acid reflux common - LOS is less competent.
describe what occurs in a rolling hiatus hernia
gastro-oesophageal junction remains in the abdomen, but a bulge of stomach herniates up into the chest alongside the oesophagus - can strangulate.
acid reflux uncommon - LOS is intact.
how would you investigate a hiatus hernia?
barium swallow.
upper GI endoscopy.
how might you manage a hiatus hernia?
weight loss, treat reflux symptoms.
surgery - if intractable symptoms, or a rolling hernia - Nissen fundoplication
give 2 conditions that predispose to inguinal hernias
male sex, chronic cough, constipation, urinary obstruction, heavy lifting, ascites, past abdominal surgery
in relation to pubic tubercle, where does an inguinal hernia present?
superior and medial
what is the difference between a direct and indirect inguinal hernia?
indirect - passes through inguinal canal into testicle due to failure in embryonic closure.
direct - enters through weak point in the transversalis fascia (the posterior wall of the inguinal canal) - Hesselbach’s triangle.
where might a lump from a femoral hernia present in a patient?
inner upper thigh, pointing down the thigh
where, in relation to the pubic tubercle, is a femoral hernia felt?
inferior and lateral
give 3 causes of an incisional hernia
infection, increased abdo pressure, poor surgical technique, obesity, haematoma
give 3 bacterial causes of infective diarrhoea
C difficile - e.g. hx of abx use (rest are travel).
shigella, salmonella, campylobacter, aeromonas, vibrio cholera.
E coli
what would you test the stool for, when investigating infective diarrhoea?
MC&S, ova cysts, parasites, C diff toxin.
give 2 viral causes of infective diarrhoea
norovirus - cruise ships etc.
rotavirus.
give 2 protozoal causes of infective diarrhoea
Giardia intestinalis
Entamoeba histolytica
Cryptosporidium parvum
Cyclospora cayetanensis
describe the pathogen that causes cholera
Vibrio cholera.
gram -ve curved flagellated motile vibrating/swarming rod.
faecal-oral spread.
describe the clinical features of cholera
profuse (1L/h) rice water stools, fever, vomiting, rapid dehydration.
how would you treat cholera?
tetracycline.
oral rehydration sachets.
how would you treat infective diarrhoea caused by salmonella, shigella or campylobacter?
ciprofloxacin oral/IV
describe the clinical features of bacillary dysentery.
abdo pain and bloody diarrhoea ± sudden fever and headache
what organism causes bacillary dysentery? how would you treat it?
shigella.
ciprofloxacin + avoid antidiarrhoeal drugs.
what type of tumours can arise from the oesophagus and where?
adenocarcinoma - lower third.
squamous carcinoma - upper 2 thirds.
name 2 risk factors for oesophageal carcinoma
smoking, alcohol, Barrett’s/GORD, obesity, achalasia, low vitamin A/C, nitrosamine exposure
give 3 symptoms of an oesophageal tumour
progressive dysphagia (initially for solids, then liquids too).
cough, weight loss, anorexia, retrosternal chest pain, dyspepsia
what would be your investigations of choice for diagnosis of oesophageal cancer, and then for staging?
endoscopic ultrasound with fine needle aspiration/biopsy of tumour.
CT for staging.
given most oesophageal cancers present late, what kind of treatment would you consider?
palliative - soft diet, oesophageal stent, analgesia - chemo/radiotherapy can be used palliatively.
what AIDS defining illness affects the oesophagus?
Kaposi’s sarcoma - found in mouth, oesophagus and hypopharynx
give 2 signs that indicate an oesophageal carcinoma is in the upper 1/3rd of the oesophagus
hoarseness and cough
give 2 differential diagnoses of oesophageal cancer
those of dysphagia
oesophagitis, diffuse oesophageal spasm, achalasia, benign oesophageal stricture
how are oesophageal cancers staged?
TNM system.
T1 = invading lamina propria
T2 = muscularis propria
T3 = adventitia
T4 = invasion of adjacent structures
what curative treatment might you attempt in a patient who has presented with early (local T1/T2) oesophageal carcinoma?
radical curative oesophagectomy + pre-op chemo with cisplatin
what is the main type of carcinoma affecting the stomach?
adenocarcinoma
give 3 things associated with gastric adenocarcinoma
pernicious anaemia, blood group A, H pylori, atrophic gastritis, adenomatous polyps, lower social class, smoking.
diet - high nitrates, salt, pickling, low vit C
what main lymph node is infiltrated in gastric tumours?
Virchow’s node (neck)
give 2 symptoms of gastric adenocarcinoma
epigastric pain relieved by food and antacids
nausea
vomiting
anorexia
weight loss
dyspepsia
dysphagia
give 2 signs of gastric adenocarcinoma
anaemia, jaundice, palpable epigastric mass with tenderness, Virchow’s node infiltration, dermatomyositis, acanthosis nigricans
in which part of the stomach do adenocarcinomas most commonly occur?
antrum
what makes up the Borrmann classification of gastric adenocarcinomas?
i. polypoid
ii. excavating
iii. ulcerating and raised
iv. diffusely infiltrative
how might gastric adenocarcinomas spread?
locally, lymphatics, blood borne (haematogenous), transcoelomic
what investigations would you perform in gastric adenocarcinoma?
gastroscopy + multiple ulcer edge biopsies.
endoscopic ultrasound.
CT for staging.
describe the treatment options for gastric adenocarcinoma
partial/total gastrectomy.
chemo - epirubicin, cisplatin, 5-fluorouracil.
surgical palliation - for obstruction, pain or haemorrage.
give 2 cell types that gastrointestinal stromal tumours (GIST)s could be
leiomyomas, leiomyosarcomas, leiomyoblastomas, Schwannomas
what are the treatment options for gastrointestinal stromal tumours?
1st line - surgical resection
2nd line - imatinib.
what is gastric lymphoma?
arises from mucosal areas from mucosa-associated lymphoid tissue - MALToma.
how would you treat a gastric lymphoma?
most are associated with H pylori - eradication.
surgery or chemo ± radiotherapy
which type of gastric polyp is pre-malginant?
adenomatous polyps.
hyperplastic polyps aren’t malignant, but can be accompanied by pre-malignant atrophic gastritis.
which types of gastric polyps are benign?
cystic gland, inflammatory fibroid polyps, hyperplastic polyps
where are adenocarcinomas and lymphomas found in the small intestine?
adenocarcinoma - duodenum and jejunum.
lymphoma - ileum.
what are the different types of lymphoma that can arise in the intestine?
Non-Hodgkin’s.
B cell, arising from MALT - polypoid masses in distal/terminal ileum.
T cell - ulcerated/strictures in proximal ileum.
what AIDS defining lymphoma can occur in the small intestine and where?
Burkitt’s lymphoma - terminal ileum of children
how might malignant small intestinal tumours be treated?
surgical excision ± chemo/radiotherapy
what autosomal dominant condition can cause benign small bowel tumours?
Peutz-Jeghers syndrome - mucocutaneous pigmentation and hamartomatous GI polyps - can undergo malignant change.
what type of cells do carcinoid tumours arise from and where in the small intestine are they found?
enterochromaffin cells, in appendix, ileum and rectum
what is carcinoid syndrome?
only occurs with liver mets, spontaneous red-blue flushing mainly on face and neck (kinins), pulmonary stenosis/tricuspid incompetence (5-HT), hepatomegaly.
tumours secrete serotonin, bradykinin, histamine, prostaglandins.
how would you treat carcinoid tumours?
somatostatin analogues - ocreotide and lanreotide.
what is a polyp? what type of lesion are most colonic polyps?
abnormal growth of tissue projecting into the intestinal lumen from the normally flat mucosal surface.
usually adenomas.
what is the clinical significance of colonic polyps?
they’re the precursor lesions of most colorectal cancer
list 3 features of an adenomatous polyp that increases the risk of malignant change
size >1cm.
sessile polys (attached to colon wall directly) > pedunculated polyps (mucosal stalk between polyp and wall).
severe dysplasia (>mild)
villous histology > tubular.
multiple polyps > singular.
what is HNPCC?
hereditary nonpolyposis colorectal cancer.
DNA mismatch repair genes are mutated.
what is the pathway of developing a colorectal cancer from a polyp?
normal epithelium => adenoma (polyp) => colorectal adenocarcinoma
how is colorectal cancer risk increased in patients HNPCC?
accelerated progression from polyps to CRC - doesn’t increase no. polyps, just speeds up their progression to malignancy.
what gene is mutated in familial adenomatous polyposis?
APC gene
how does FAP increase risk of colorectal cancer?
patient develops loads and loads of colorectal polyps in teenage years - increased risk of extracolonic malignancies.
100% lifetime risk of CRC, onset in young adults.
how can colorectal cancer be prevented in people with FAP?
regular screening from age of 12, prophylactic total colectomy at 20.
what other cancers, apart from CRC, are associated with FAP?
thyroid, pancreatic and hepatoblastomas.
give 3 risk factors of colorectal carcinoma
increasing age, obesity, IBS, diabetes, obesity, alcohol, FHx, colorectal polyps, low fibre diet, genetic predisposition (FAP. HNPCC), smoking, UC and Crohn’s
explain the different clinical features of right and left sided colorectal carcinomas
left - PR bleeding/mucus, obstruction, tenesmus, PR mass.
right - weight loss, anaemia, abdo pain, usually asymptomatic.
either - abdo mass, perforation, haemorrhage, fistula
what is the gold standard investigation in colorectal carcinoma?
colonoscopy with biopsy
describe the UK bowel cancer screening programme
all >60yrs has faecal occult blood testing every 2yrs - positive result = endoscopy.
which parts of the colon/rectum are most commonly affected by colorectal cancer?
rectum - 27%.
sigmoid colon - 20%.
caecum - 14%
what are the urgent referral criteria for bowel cancer?
1) over 40 with PR bleeding and change in bowel habit
2) any age with R lower abdo mass
3) palpable rectal mass
4) men/non-menstruating women with unexplained iron deficiency anaemia
explain the Dukes’ criteria system for staging colorectal carcinoma
A - limited to muscularis mucosae
B - extension through muscularis mucosae
C - involvement of regional lymph nodes
D - distant metastases
what is generally the treatment for colorectal carcinoma?
surgical resection followed by post-op chemo/radiotherapy.
name 2 PPIs
lansoprazole, omeprazole, pantoprazole
how do PPIs work?
reduce gastric acid secretion by irreversibly inhibiting H+/K+ ATPase in gastric parietal cells - this is the proton pump responsible for secreting H+.
suppresses gastric acid production almost completely.
give an example of an H2 receptor antagonist
ranitidine
why are H2 receptor antagonists not as good at suppressing gastric acid secretion as PPIs?
blocking the H2 receptor reduces the activation of the proton pump - but the pump can be activated by other pathways, so does not completely suppress secretion like PPIs do.
how does loperamide work?
agnoist of the opioid mu-receptors in GI tract - increases non-propulsive contractions of the gut smooth muscle, but reduces peristaltic contractions.
transit of bowel content is thus slowed, and anal sphincter tone is increased - more water absorbed from faeces as there’s more time for this, so stools are hardened.
give 2 examples of aminosalicylates - what are they used for?
mesalazine - UC.
sulfasalazine - UC + RA.
how do aminosalicylates work to treat UC?
release 5-ASA, which has anti-inflammatory and immunosuppressive effects and acts topically on the gut.
name an antimuscarinic with a GI use - what disease is used to treat and why?
hyoscine butylbromide - first line for IBS, used for their antispasmodic effects.
how do antimuscarinics work in the gut?
bind to muscarinic ACh receptor and competitively inhibit ACh - increase in peristaltic contraction and reduction in smooth muscle tone, and reduced gut secretions - opposite to parasympathetic rest and digest effects.
name an acetylcholinesterase inhibitor with a GI indication and what it is used for?
neostigmine - used for pseudoobstruction of the colon.
how does neostigmine work?
it is a reversible acetylcholinesterase inhibitor - increases about of ACh available to stimulate both nicotinic and muscarinic receptors - produces muscle contraction to restore bowel motility.
how does ursodeoxycholic acid work?
reduces cholesterol absorption and is used to dissolve cholesterol gallstones.
it’s a bile acid that is present in the body anyway.
how does cholestyramine work?
binds bile in GI tract to prevent its reabsorption by forming insoluble complexes with bile acids, which are then excreted in the faeces.
useful for pruritus in primary biliary cirrhosis/liver failure.
also reduces plasma cholesterol levels.
vasoconstrictors such as terlipressin are used to medically manage bleeding oesophageal varices, how do they stop the bleeding?
analogue of vaopressin, which itself causes vasoconstriction - reduced blood flow to the area.
imatinib is used when surgery isn’t an option for treatment of gastric stromal tumours - how does it work? what haematological disorder is it the principal treatment for?
it’s a tyrosine kinase inhibitor, so blocks the transfer of a phosphate group from ATP to a protein in a cell.
cell cannot proliferate.
also used to treat CML.
why are somatostatin analogues used to treat carcinoid syndrome?
carcinoid tumours release hormones including serotonin, bradykinin etc.
somatostatin analoges inhibit the release and action of these hormones.
which types of oesophageal cancer occur in the upper 2/3rd and lower 2/3rd?
upper 2/3rd - squamous carcinoma
lower 1/3rd - adenocarcinoma
