GI Flashcards
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
NOT h. pylori!
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, increased saliva production (water brash), odynophage (painful swallowing), acid brash (retrosternal discomfort from regurg. of acid/bile)
give 2 extra-oesophageal / atypical features of GORD
nocturnal asthma, chronic cough, laryngitis (hoarseness, throat clearing), sinusitis, *non-cardiac chest pain
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/dyspepsia. 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 (dysphagia)
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.
stop drugs if causing the problem.
OTC antacids.
how might you manage GORD, beyond lifestyle changes?
antacids or alginates.
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/malaena/collapse due to hypovolaemia via an oesophageal mucosal tear.
linear mucosal tear at oesophageo-gastric junction.
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 (80%), gastric (20%)
what two things cause most peptic ulcers?
H. pylori - vast vast majority.
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 if >55yo or ALARMS - biopsy to exclude malignancy.
C13-urea breath test for H pylori ± stool antigen test - immunoassay using monoclonal antibodies.
FBC for IDA.
if NSAID and H.Pylori -ve biopsy for ?Zollinger-Ellison (gastrin secreting tumours in duodenum)
how would you treat an H pylori +ve peptic ulcer patient?
triple therapy eradication regime for 1 week = PAM/PAC = PPI + amoxicillin + clarithromycin/metronidazole
or - PPI for 4/52
how would you treat an H pylori -ve peptic ulcer patient?
stop aspirin/NSAIDs, or make sure being taken after food.
PPIs - lansoprazole (or rantidine - H2 blocker) - 8 weeks.
smoking cessation.
give 2 possible complications of peptic ulcer disease
perforation (surgical closure, drain abdo) - acute abdo/peritonism.
bleeding (haematemesis/malaena)
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 - see UGIB management.
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 investigations would you do in achalasia? findings?
manometry = gold standard - high resting pressure and incomplete relaxation on swallowing.
barium swallow - lack of peristalsis and **swan neck/beak deformity at lower oesophagus
on CXR may see vastly dilated oesophagus behind the heart.
what cosmetic drug might help a patient with achalasia?
botulinum toxin A (botox) - injected into LOS
what surgical treatments are available to treat achalasia? medical management?
endoscopic balloon dilation or Heller’s cardiomyotomy (surgical division of LOS) - risk of perf.
medical = CCB/nitrates can help but can lead to GORD.
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 dyspepsia symps 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?
immune mediated gluten-sensitive enteropathy.
T cell mediated autoimmune disease.
abnormal jejunal mucosa that improves when gluten is removed and relapses when gluten is reintroduced.
gluten = wheat, rye, barley.
explain the pathogenesis of coeliac disease
genetics = HLA-DQ2/DQ8.
alpha gliadin (protein from gluten) passes through damaged epithelium of small intestine - deaminated by tissue transglutaminase. immune reaction at HLA-DQ8 produces toxic 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. anaemia (mouth ulcers, angular stomatitis, iron/B12/folate).
80% present non-classically = IBS, bloating/fullness, *chronic fatigue.
skin fx = dermatitis herpetiformis - blistering on arms, legs, buttocks
neuro fx = cerebellar ataxia, peripheral neuropathy, dementia, depression.
other fx = amenorrhoea, subfertility.
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?
antibodies: IgA anti-tissue transglutaminase (tTG IgA) antibodies, anti-enodmyseal antibodies (anti-EMA IgA)
- FBC = anaemia (iron/folate).
- LFT = should normalise on gluten free diet, if not consider autoimmune HPB diseases
what is the gold standard investigation for coeliac disease? what will it show?
4x biopsy from second part of duodenum onwards (small bowel) via endoscopy.
shows subtotal villous atrophy and crypt hyperplasia.
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 NOT avoid gluten in 6W leading up to Ix - will be falsely negative.).
avoid - wheat, rye and barley.
gluten-free biscuits, flour, bread and pasta are prescribable. give info on foods, websites, Coeliac UK, ?Ca/vit D supplements.
offer annual review.
consider DEXA scan for osteoporosis.
give 2 possible complications of coeliac disease
anaemia, secondary lactose intolerance, increased risk of malignancy, osteoporosis, infertility
anxiety, depression*
what is tropical sprue?
malabsorptive disease of small bowel characterised by inflammation and villous atrophy, in individuals from tropical areas where it’s endemic (SE Asia, Caribbean)
describe the pathological features of tropical sprue
jejunal biopsy shows incomplete villous atrophy/flattening
FBC = macrocytic anaemia due to B12/folate deficiency
low potassium/iron/albumin due to malabsorption/diarrhoea.
check stool for cysts, ova, parasites.
how does tropical sprue present?
diarrhoea, steatorrhoea, megaloblastic anaemia
how would you treat tropical sprue?
fluid replacement
tetracycline for 6/12 + folic acid/B12 supplements
don’t supplement iron when on tetracycline (without chelation at least)
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 (75%), strangulated hernia, malignancy, volvulus.
large bowel - colorectal carcinoma if pt >70 (risk increases with cancer further down as faeces more solid), diverticular strictures, sigmoid 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
abdo distension (larger the lower the lockage)
what can be heard on examination in both large and small bowel obstruction?
tinkling bowel sounds
silent bowel = ileus.
how might you manage large/small bowel mechanical obstruction?
small/uncomplicated may settle with conservative management - NG tube + IV fluids (‘drip & suck’).
large/unclear diagnosis = laparotomy, consent for stoma. urgent surgery if peritonitis/evidence of perforation.
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
(“ileus” = non-mechanical obstruction)
post-op ileus = due to handling of bowel.
give 3 possible causes of paralytic ileus
surgery, pancreatitis/peritonitis, spinal injury, hypokalaemia, hypnoatraemia, uraemia, peritoneal sepsis, tricyclic antidepressants
tend to be elderly with multiple comorbidities.
absent bowel sounds! AXR shows fluid levels.
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
can be acute or chronic, or can also get ischaemic colitis which affects the colon.
give 3 causes of acute mesenteric ischaemia
superior mesenteric artery thrombosis/embolism, non-occlusive disease, trauma, vasculitis, radiotherapy, strangulation
how does acute mesenteric ischaemia present?
acute severe colicky, poorly localised abdominal pain, no abdominal signs, rapid hypovolaemia leading to shock.
*pain out of proportion to symptoms, no tenderness/peritonitis.
how do you investigate acute mesenteric ischaemia?
gold standard = angiography.
AXR - for obstruction, ileus, thickened bowel, *thumbprinting (oedema and inflammation)
what is the main complication you would be worried about in a patient with acute mesenteric ischaemia?
septic peritonitis - possible progression of SIRS to multi-organ dysfunction syndrome
what antibiotics would you give to a patient with acute mesenteric ischaemia?
gentamicin + metronidazole
how would you treat acute mesenteric ischaemia?
ABCDE, resus with O2/fluids etc.
- papaverine relieves spasm, heparin for the thrombus.
- surgical angioplasty to superior mesenteric artery
mortality 90%
what vessel is blocked in ischaemic colitis?
superior mesenteric artery - from middle colic artery to transverse (2/3rd)
inferior mesenteric artery supplies left colic artery to descending
how might a patient with ischaemic colitis present?
sudden onset abdominal (LIF) pain, metabolic acidosis. passing bright red blood.
what characteristic feature would you see on abdo XR/barium enema in a patient with ischaemic colitis?
other Ix?
‘thumb printing’ of splenic flexure if in early phase, due to oedema (not sure if this is abdo XR or barium enema).
colonoscopy shows blue swollen mucosa.
how would you treat ischaemic colitis?
fluid replacement + abx/bowel rest/supportive care - most recover, left with strictures
give 2 risk factors of ischaemic colitis
thrombotic/embolic risk factors - vasculitis, *the Pill, *cocaine, thrombophilia
decreased cardiac output, shock, trauma, coag disorders
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 - usually above this line.
give possible causes/RFs of haemorrhoids
constipation with prolonged straining.
congestion from pelvic tumour, pregnancy, CCF, portal hypertension.
RFs = constipation/prolonged straining, increased abdo pressure (ascites, pregnancy, chronic cough).
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.
refer 2WW if suspect anal cancer!
describe the management options for haemorrhoids
prevent constipation - fibre, fluid, bulk forming laxative.
topical anaesthetics.
rubber band ligation = grade 2.
sclerosants - phenol injected into the pile.
infra-red coagulation.
surgical - excision haemorrhoidectomy, stapled haemorrhoidopexy - if large, refractory, v. painful.
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.
Ix = MRI.
what are anal fissures? presentation?
painful tear in squamous lining of the lower anal canal
pain on defecation (shards of glass) - bright red blood on stool or paper.
give 2 causes of anal fissures
hard faeces/constipation. IBD, esp. Crohn’s.
other - syphilis, herpes, trauma (e.g. childbirth, FBs), anal cancer, psoriasis
how would you treat anal fissures?
conservative = dietary fibre, increase fluid intakes.
local anaesthetic ointments (lidocaine/GTN) or topical diltiazem, laxatives (adults - bulk-forming ispaghula husk (?), child = osmotic e.g. lactulose).
2nd line - botulinum toxin injection, or lateral internal sphincterotomy.
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 usually?
obstruction of natal cleft hair follicles with ingrowing hair
list some diseases that perianal abscess could be the first feature of - other causes of perianal abscess?
Crohn’s, UC, TB.
causes - infection of fissure, STI, blocked anal gland.
60% due to direct extension of sepsis in intersphincteric plane.
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?
6/12 hx of ABC (abdo pain, bloating, change of bowel habit) + abdo pain/discomfort relieved by defecation or assoc w/ 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 (IBD) and coeliac antibody screen (for EMA and TTG), Ca-125 (ovarian Ca)
may also do - TFT, faecal occult blood, colonoscopy.
how would you manage IBS?
diet - avoid fibre, fructose, wheat, starch, caffeine, alcohol, stress reduction, physical activity, high fibre foods, drink enough fluids etc
medications - but aim for lifestyle Rx!
constipation = biscodyl and sodium picosulphate (laxatives).
diarrhoea - bulking agent ± loperamide after each loose stool.
colic/bloating - antispasmodics - buscopan (hyoscine butylbromide) mebervine, simeticone etc
psychological therapies
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 some possible complications of diverticulitis
POFAS (1/3rd pts will get one) = perforation, obstruction, fistula, abscess, stricture.
also haemorrhage - common cause of LGI (abrupt painless bleeding or cramps w/urge followed by large amount of blood - usually stops on its own)
how would you treat diverticulitis?
?admit/NBM if suspect will need surgery (30% will) e.g. pain uncontrolled with paracetamol, hydration not maintained, sig. bleeding (requiring fluid/blood resus), perforation.
if managing at home - broad-spec abx (Co-amoxiclav) for 7 days, paracetamol.
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 (ascites associated with spontaneous bacterial peritonitis (SBP) - also caused by intraperitoneal dialysis bacteria)
females, immunocompromised, peritoneal dialysis, ascites.
give 3 examples of causes of secondary peritonitis
any pathological process adjacent to peritoneum that causes inflammation:
e.g. *perforation, inflammation of abdo organs, peritoneal dialysis, TB, ischaemia of abdo organ, chemical.
how does peritonitis usually present?
pain + anorexia + N&V, deteriorating patient.
O/E - high fever, tachycardia, tenderness on palpation, guarding, rebound tenderness, rigidity, silent abdomen, patient lies very still
what investigations would you perform on a patient with peritonitis/intra-abdo abscess?
FBC, U&E, LFT, amylase, lipase, **blood culture, might aspirate peritoneal fluid.
imaging - AXR, CXR (free air under the diaphragm)
how would you manage peritonitis/intra-abdo abscess?
ABCDE!
abscess = broad spec abx, metronidazole + 3rd gen cephalosporin + surgical drainage. peritonitis = support with IV fluid, IV abx (met + cefotaxime) then open/laparoscopic surgery.
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?
CXR
barium swallow.
upper GI endoscopy.
how might you manage a hiatus hernia?
weight loss, treat reflux symptoms etc - lifestyle advice as per GORD. long term PPI.
surgery - if intractable symptoms, or a rolling hernia - Nissen fundoplication, and/or gastropexy.
in relation to pubic tubercle, where does an inguinal hernia present?
superior and medial
presents as lump ± pain (± incarceration)
indirect can cause pain/dragging sensation in scrotum
what is the difference between a direct and indirect inguinal hernia?
indirect (80%) - passes through inguinal canal (via deep inguinal ring ± superficial inguinal ring) into testicle due to failure in embryonic closure - more likely to strangulate!
direct - enters through weak point in the transversalis fascia (the posterior wall of the inguinal canal) - Hesselbach’s triangle - easily reduced.
where might a lump from a femoral hernia present in a patient?
inner upper thigh, pointing down the thigh
more common in women than men.
swells on cough or strain, pain if incarcerated.
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
req. urgent repair with reinforced mesh if large/
how would you manage a pyogenic abscess?
percutaneous aspiration under radiological (e.g. US) control.
pig tail catheter for continuous drainage.
IV metronidazole and cefuroxime.
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 types of tumours are most common in which parts of the oesophagus?
adenocarcinoma - lower third.
squamous carcinoma - upper 2 thirds.
name 2 risk factors for oesophageal carcinoma
bother - smoking*, alcohol
AC - Barrett’s/GORD, obesity, other GORD RFs
SCC - chronic inflammation and stasis e.g. achalasia
what are the red flags in history that make you worry about oesophageal cancer?
***progressive dysphagia (initially for solids, then liquids too).
- vomiting
- weight loss + anorexia
- symps of occult GI bleeding e.g. malaena
- symps of infiltration eg. intractable hiccups, persistent retrosternal pain.
hoarseness/cough is specific to upper 1/3rd but less common.
also lymphadenopathy.
investigations for oesophageal cancer?
endoscopy with brushing and biopsy of lesion.
- FBC, U&E, LFT, glucose, CRP
CXR for mets
CT for staging.
double contrast barium swallow for dysphagia.
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 dysphagiaoesophagitis, 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? which areas of the stomach does it generally occur?
adenocarcinomas
gastric cancer usually occurs in: 50% pylorus, 25% lesser curve, 10% cardia, 5% lymphoma
5th most common cancer worldwide, 2nd most common cancer death. Japan, China = most common.
give some RFs for gastric cancer
- age (95% >55yrs)
- Male (2:1)
- H. pylori
- diet - salt, *pickling, low vit C/fruit +veg
- smoking
- *blood group A
- atrophic gastritis, pernicious anaemia
- familial risk - E-cadherin gene mutation
- *nitrosamines exposure
what main lymph node is infiltrated in gastric tumours?
Virchow’s node (left supraclavicular)
enlargement = Troisier’s sign - metastatic abdo malignancy. NOT GOOD.
how does gastric cancer tend to present? red flags?
vague - dyspepsia, wt loss, vomiting, dysphagia, anaemia
red flags as for dyspepsia (ALARMS).
most present late!!
what signs suggest a gastric cancer is likely to be incurable
palpable epigastric mass, hepatomegaly/jaundice (liver mets), Troisier’s sign (Virchow’s node)
what makes up the Borrmann classification of gastric adenocarcinomas?
i. polypoid
ii. excavating
iii. ulcerating and raised
iv. diffusely infiltrative
by what different routes can gastric cancers spread?
locally, lymphatics, blood borne (haematogenous), transcoelomic *to ovary = Krukenberg’s tumour.
to lung and liver most common.
what investigations would you perform in gastric cancer?
flexible endoscopy/gastroscopy + multiple ulcer edge biopsies.
biopsy shows *signet ring cells
spiral CT abdo/thorax for staging.
FBC for anaemia, LFT for liver involvement.
describe the treatment options for gastric cancer
- nutritional support/deficiency screen + symptom control (pain, nausea, constipation etc)
- surgery - distal tumour = subtotal gastrectomy, proximal = total gastrectomy if within 5cm of OG junction.
- peri-op chemo = 5-FU
palliative chemo - epirubicin, cisplatin, 5-fluorouracil.
blood transfusion for symptomatic anaemia.
what cell types can gastrointestinal stromal tumours (GIST)s be? where in GI tract do these occur? cause?
leiomyomas, leiomyosarcomas, leiomyoblastomas, Schwannomas
these are soft tissue sarcomas, usually caused by oncogenic kinase mutation = 80% have KIT receptor tyrosine kinase mutation. also associated with neurofibromatosis T1.
50% occur in stomach, 25% in small bowel, 10% colon/rectum
how do GISTs present? Ix/Rx?
pres - early satiety, bloating, fever, wt loss, night sweats, *GI bleeds.
Ix - often incidental finding on CT. do CT chest, abdo and pelvis, ?MRI. DON’T biopsy if it’s resectable.
Rx - all have potential to become malignant, if aggressive mets to liver.
1st line - complete surgical resection (handle carefully to avoid rupture and dissemination)
2nd line - imatinib (tyrosine kinase inhibitor) - often used adjuvantly
what are MALT lymphomas?
arises from mucosal areas from mucosa-associated lymphoid tissue - MALT lymphoma.
subtype of NHL - extranodal marginal site lymphoma.
lymphoid proliferation in MALT rather than lymph nodes, so follow a different course to nodal B cell lymophomas.
1/3rd are gastic - associated w/ H. pylori - dyspepsia, pain, ulcer, fever, wt loss etc.
C. jejuni infection causes it in small bowel.
non gastric = head, neck, lung, eye.
how would you treat a gastric MALT lymphoma?
usually indolent and confined to stomach.
endoscopy + gastric biopsy shows prominent follicles surrounded by lymphocytes.
?bone marrow biopsy/phenotype circulating lymphocytes.
early stage = H pylori eradication. + endoscopic F/U
locally advanced/high grade = + rituximab (anti CD20 B cell MAb (monoclonal Ab)) + chemo + radio
refractory = surgery, ideally aim for gastric preservation.
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
red/processed meat.
explain the different clinical features of right and left sided colorectal carcinomas
left - PR bleeding/mucus, obstruction, tenesmus, PR mass, colicky pain, *less advanced at presentation.
right - weight loss, anaemia, occult bleeding abdo pain/mass in RIF, usually asymptomatic.
general presentation = change in bowel habit, rectal bleeding + anaemia.
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 = colonoscopy.
which parts of the colon/rectum are most commonly affected by colorectal cancer?
2/3rd = colon, 1/3rd = rectum. 40% = rectum + sigmoid.
what are the urgent referral (2WW) criteria for bowel cancer?
1) over 40 with PR bleeding and change in bowel habit for >6W
2) >60yrs with rectal bleed alone
non 2WW referral:
- R lower abdo mass
- palpable rectal mass
- men/non-menstruating women with unexplained iron deficiency anaemia
explain the Dukes’ criteria system for staging colorectal carcinoma
(5 yr survival %)
A - limited to muscularis mucosae (90%)
B - extension through muscularis mucosae/serosa (70%)
C - involvement of regional lymph nodes (30%)
D - distant metastases/liver mets (5%)
what is generally the treatment for colorectal carcinoma?
surgical resection followed by post-op (R/L hemicolectomy + LN clearance)
chemo - FOLFOX (folinic acid + fluorouracil + oxaliplatin)
F/U = 2xCT scan + 6mthly CEA in first 3 yrs.
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 carcinomalower 1/3rd - adenocarcinoma
give some risk factors for inguinal hernias
obesity, constipation, chronic cough, heavy lifting, male
how can you distinguish between a direct and indirect inguinal hernia on examination?
reduce the hernia and occlude the deep inguinal ring, palpate for lump appearing when coughing.
if it stays reduced = indirect hernia.
if in doubt, USS can help.
describe where the deep and superficial inguinal rings are?
DIR = halfway point of the inguinal ligament SIR = split in external oblique aponeurosis, superior and lateral to pubic tubercle
how do you manage an inguinal hernia?
if small - watch and wait, warn of risk of becoming surgical emergency (obstruction and incarceration).
advise - stop smoking, weight loss, diet.
surgical reduction, or excision of hernial sac + closure of defect with minimal tension (mesh).
how do you differentiate between femoral hernia and hydrocele?
can get above a hydrocele O/E, can’t with a femoral hernia.
how does a strangulated hernia present?
red, tender, tense, irreducible ± colicky abdo pain + vomit + distension
(obstruction = surgical emergency)
management of a femoral hernia?
all should be repaired as have high strangulation rate (herniotomy)
what are the different types of hernia?
inguinal (direct v indirect)
femoral
incisional
epigastric (midline, above umbilicus, surgical repair essential due to strangulation risk)
umbilical - congenital or associated w/ascites etc.
what’s the ROME criteria for functional dyspepsia?
6/12 post-prandial fullness
early satiety
epigastric pain/burning
no evidence of structural disease on endoscopy
what 4 main groups of drugs can cause dyspepsia?
1) nitrates
2) bisphosphonates
3) corticosteroids
4) NSAIDs - decrease mucus and bicarbonate secretion
what investigations might be useful in dyspepsia?
- FBC (checks for anaemia as part of ALARMS red flags)
- H. pylori tests (C13 urea breath tests, stool antigen test + CLO test - must stop PPI/abx 2/52 before)
- upper GI endoscopy if ALARMS or >55 (2WW)
- barium swallow might be used
what are the five areas of the stomach?
cardia fundus body antrum pylorus
what are the different cell types in the stomach? what does each one produce?
- chief cells = pepsinogen (converted to pepsin by HCl)
- G-cells = gastrin (in antrum)
- parietal cells = intrinsic factor and HCl (fundus + body)
- D-cells = somatostatin (antrum)
- Goblet cells = mucus + bicarbonate
what hormones/neurotransmitters etc stimulate vs stop acid production in the stomach?
stimulate = gastrin (CCK-2), histamine (H2), ACh (M3)
stop = stomatostatin
briefly describe acid production in the stomach
CO2 and Cl diffuse to cell from blood
CO2 + H20 (carbonic anhydrase) -> H2CO3 -> H+ + HCO3-
H+ combines with Cl, ATP pump to pump to duct (as HCl more conc)
cAMP increased by gastrin, histamine, ACh to pump more acid
give some info on how H. pylori infection affects the GI system.
gram -ve curved bacillus.
causes vast majority of PUD, and x6 risk of gastric adenocarcinoma.
passes through mucus layer, secretes urease which works to neutralise stomach acid –> mucosal cell death, chronic inflammation –> ulceration.
uses iron for its own growth, and decreases vit C, and causes micro-erosions/chronic bleeding — all contributes to causing IDA.
what investigations might you do for GORD?
gold standard = endoscopy (if >55, ALARMS - 2WW referral!)
FBC = excl. anaemia.
barium swallow - if considering hiatus hernia.
oesophageal pH monitoring.
what is a hiatus hernia? RFs?
herniation of part of abdo viscera through oesophageal aperture of diaphragm - usually gastric cardia.
RFs = things that increase intra-abdominal pressure e.g. obesity, pregnancy, ascites, advanced age
briefly describe the structure of the oesophagus (incl blood supply, muscle type, epithelium)
- upper 1/3 = inferior thyroid, voluntary striated muscle, stratified squamous epithelium
- middle 1/3 = aortic and oesophageal, mixed muscle, stratified squamous
- lower 1/3 = left gastric, smooth muscle, columnar
what is oesophagitis? how is it graded? management?
similar to GORD, can be a progression of it.
grading = on endoscopy using Los Angeles grading:
- A = 1+ mucosal breaks <5mm, none extending between tops of mucosal folds
- B = as for A but >5mm
- C = mucosal breaks extending between tops of 2+ mucosal folds, involving <75% of mucosal circumference
- D = mucosal breaks involve >75% of mucosal circ.
Rx = 2/12 PPI
outline management of Barrett’s oesophagus?
low grade = lifestyle as for GORD + long term PPI ± ablation
high grade = oesophagectomy.
give some oesophageal causes of dysphagia
- GORD
oesophagitis, oesophageal cancer (feels like food sticking, solids»_space; liquids), pharyngeal cancer
give some neuro and some ‘other’ causes for dysphagia
neuro = CVA, achalasia, diffuse oesophageal spasm, MS, MND
others = pharyngeal pouch, external compression (mediastinal tumour), CREST or scleroderma
list some common causes of a UGIB
peptic ulcer - most common
oesophagitis, gastritis
*varices, Mallory-Weiss tear, malignancy, drugs
how might an UGIB present?
- haematemesis = bright red/fresh implies above stomach bleeding, active haemorrhage; coffee ground = stomach or below.
- malaena = black tarry stools, typical smell - usually UGIB, can be small bowel. - iron supplementation can lead to dark stools which might be mixed up with malaena
- haematochezia = passing blood PR - usually lower GI problem if fresh blood.
- abdo pain
- fx of underlying cause e.g. dyspepsia, wt loss, jaundice
how would you assess and Ix someone with an UGIB?
ABCDE, Iv access etc etc
- want to establish extent of blood loss and degree of shock.
- look for pallor and signs of anaemia.
- postural hypotension implies blood loss of >20%.
Ix - endoscopy post resus/within 24h.
FBC 4hrly. crossmatch blood 2-6 units. ?major haemorrhage protocol?
coag profile, LFT, test renal function.
CXR/erect and supine AXR
initial management of an UGIB?
if shock = fluid resus, high flow O2.
2x wide bore cannula, send bloods (FBC/UE/LFT/cross match/coag)
fluid bolus 500ml over 15 mins (up to 2L).
? active major haemorrhage protocol - bloods, FFP, platelet transfusions.
then - CXR, ECG, ABG, catheter, regular monitoring. endoscopy.
what’s involved in the Rockall score for UGIB mortality?
used pre-endoscopy for mortality (/7):
- age: 60-80 = 1, 80+ = 2
- shock: tachy >100 = 1, hypotensive = 2
- comorbidity: heart (IHD, HF) = 2, renal/liver/malignancy = 3
post-endoscopy to assess re-bleed (/11), < 3 is low risk:
- Dx: MW tear/no bleeding (0), all other (1), malig. (2)
- blood visible: no blood or dark spot (0), clot/bleed (2)
management of UGIB according to Dx?
Non-variceal bleeds e.g. PUD:
- endoscopic treatment - mechanical clips, thermal coagulation + adrenalin, fibrin/thrombin with adrenaline.
Variceal bleed: terlipressin at presentation, prophlactic abx.
- oesophageal = band ligation
- gastric = endoscopic injection of butyl cyanoacrylate ± TIPS (transjugular intrahepatic portosystemic shunt)
what classic X ray sign is seen in sigmoid volvulus?
coffee bean sign - grossly dilated sigmoid loop.
typical presentation of sigmoid volvulus? management?
presents - elderly, chronically constipated (large atonic bowel), ± megacolon ± hx of sigmoid volvulus, with sudden onset colicky lower abdo pain + gross abdo distension + **failure to pass flatus/stool.
palpable mass O/E + tympanic distended abdo.
urgent admit - AXR/CT scan, decompression w/ sigmoidoscope + placement of flatus tube alongside (in place for 24hrs).
if recurrent - elective resection of sigmoid colon.
how does an abdominal abscess present?
classically get a swinging fever ± palpable mass.
fever + pain.
describe the grading of haemorrhoids
grade 1 = no prolapse
grade 2 = prolapse on strain, reduce spontaneously
grade 3 = prolapse on strain, reduce manually
grade 4 = permanent prolapse
what is a Meckel’s diverticulum?
- remnant of the vitellointestinal duct at the distal ileum.
- asymptomatic or can cause haemorrhage
- usually in kids <2yrs, or if presenting with intestinal obsutrction.
- always consider in DDx of rectal bleed or intestinal obstruction.
what is chronic mesenteric ischaemia? Ix/Rx?
“intestinal angina” - due to chronic atherosclerosis in superior mesenteric artery.
presentation - wt loss, postprandial pain, fear of eating.
Ix - angiography is gold standard.
Rx - nitrate therapy, anticoagulate, ?bypass surgery
list some investigations that might be done if you were blind testing for malabsorption (/causes of)
- FBC, LFT, ESR, CRP
- Iron studies (ferritin), folate, B12
- albumin and corrected calcium
- clotting screen + INR (vit K)
- *anti-endomysial, anti-reticulin, alpha-gliadin
- stool - faecal elastase (A1AT), MC&S
- abdo USS - gallbladder, liver, pancreas
- barium studies (structural causes)
- endoscopy + biopsy
list some signs/symps of malabsorption, according to the micronutrient they’re deficient in
steatorrhoea = foul, floating, pale
- iron/folate/B12 = pallor/glossitis
- Vit A = hyperkeratosis/scaliness
- Vit D/Ca = bones/stones/moans/groans
- Vit K = bleeding
what conditions are associated with coeliac disease?
T1DM
autoimmune thyroid disease
metabolic bone disease
Down’s, Turner’s.
primary biliary cirrhosis, primary sclerosing cholangitis.
autoimmune hepatitis.
describe the grading system used in coeliac disease
Marsh criteria looks at lymphocytes, crypts and villi on histology:
I - increased interaepithelial lymphocytes (IILC)
II - IILC and crypt hyperplasia (CH)
IIIa - IILC + CH + partial villous atrophy
IIIb - IILC + CH + subtotal villous atrophy
IIIc - IILC + CH + total villous atrophy
when would you do a 2WW referral for gastric cancer?
immediate referral if acute GI bleed!!
any age 2WW - dyspepsia + dysphagia/wt loss/vomiting/IDA/mass
> 55yrs 2WW = recent onset dyspepsia
other 2WW = worsening dyspepsia + suspect Barrett’s oesophagus/atrophic gastritis (e.g. pernicious anaemia)
what’s the Amsterdam criteria for HNPCC?
3-2-1
- 3+ relatives w/ associated Ca (CRC, endometrial, small intestine, ureter)
- 2+ successive generations
- 1 before 50
- FAP excluded
what investigations might you do in CRC?
- PR exam + colonoscopy + biopsy of lesion
- FBC and LFT (anaemia/liver mets)
- flexi sig (detects 60%)
- CEA blood tests - carcinoembryonic antigen
- stool sample for faecal occult blood
- CT abdo/thorax/pelvis for mets + liver USS
how do you distinguish Crohn’s vs UC macrocytically?
CD = rectal sparing, skip lesions, mucus cobblestoning UC = non-rectal sparing, continuous disease, ulcers, polyps
how do you distinguish Crohn’s vs UC microcytically?
CD = transmural inflammatory cell infiltrate, granuloma, focal crypt abscess, increased goblet cells
UC = inflammatory cell infiltrated confined to mucosa and submucosa, focal crypt abscess, goblet cell depletion
how do you distinguish Crohn’s vs UC on barium study?
CD = rose thorn ulcers, kantors string sign
UC = loss of haustrations, narrow short colon (lead pipe colon)
