GI Pathology Flashcards
What are the types of mucosa along the GI tract?
Oesophagus - stratified squamous (white)
Stomach - thick glandular (red brown)
Small intestine - glandular with villi
Colon and rectum - glandular with crypts
What is GORD
regurgitation of the acidic gastric contents into the lower oesophagus. the acid injury the squamous epithelium lining the oesophagus and results in inflammation
what are risk factors for GORD?
obesity
pregnancy
smoking, alcohol, coffee
hiatus hernia
What are complications and presentation of GORD?
regurgitation of acid contents into the mouth - water brash
oesophgitis - heart burn
barretts oesophagus
stricture - progressive dysphagia
bleeding - peptic ulcer may bleed. large bleeds may present with haematemesis or meleana. multiple smaller bleeds over time may present as anaemia.
What is Barrett’s oesophagus?
occurs in approx 10% of patients with long standing GORD.
metastatic process in the lower oesophageal mucosa.
it is an adaptive response to prolonged injury caused by GORD.
it is ASYMPTOMATIC and most cases are identified when patients undergo GI endoscopy for evaluation of upper GI symptoms such as GORD or dyspepsia.
How many Barrett’s Oesophagus patients progress to invasive adenocarcinoma?
2%
Oesophageal cancer epidemiology
most common in the 50-70y age group
M>F
Oesophageal cancer presentation
presents as progressive dysphagia from solids to liquids
non specific B symptoms
Investigation of oesophageal cancer
endoscopy and biopsy
what are the most common types of oesophageal cancer?
- adenocarcinoma
2. squamous cell carcinoma
how is oesophageal cancer staged?
TNM system
how is oesophageal cancer managed?
discussed at MDT meeting
curative intent - surgery with or without neoadjuvant therapy
palliative therapy - dilatation, stenting, radiotherapy etc
what is the prognosis of oesophageal cancer?
very poor
5-10% 5y survival
usually presents late
what is gastritis?
inflammation in the stomach
causes of gastritis
NNSAIDs
H.Pylori infection
what is H Pylori
gram negative bacteria that colonises the stomach
read by oral-oral or fecal-oral
lives in thick mucus layer on the mucosal surface
synthesises urease which catalyses the conversion of urea to ammonia, which neutralises the gastric acid and thus improves survival of the bacteria
what are the consequences associated with h.pylori infection?
more than 80% have an asymptomatic mild chronic gastritis
minority develop symptomatic gastritis
minority develop a peptic ulcer
small minority develop gastric carcinoma
very small minority develop gastric lymphoma
what is a peptic ulcer
a breach in the mucosa of the lower oesophagus, stomach and duodenum which fails to heal over a reasonable period of time
most commonly located in the gastric antrum or proximal duodenum
by definition, the breach extends through the full thickness of the mucosa. it MAY extend into the submucosa or deeper layers of the wall
what are the commonest causes of gastric and duodenal peptic ulcers?
h pylori
NSAIDs
other contributory factors:
alcohol, smoking, stress
what is a stress (curling) ulcer?
seen in patients with massive trauma, extensive burns, sepsis, raised ICP or shock.
thought to arise as a consequence of mucosal ischaemia leading to increased susceptibility to acid pepsin injury
what is the MOST common cause of oesophageal peptic ulcers?
GORD
the three factors of chronic inflammation
persistent tissue injury
ongoing inflammatory response
attempts to heal by fibrosis/scar formation
complications of peptic ulcers
bleeding
perforation
stricture formation
malignant change
epidemiology of gastric cancer
peak incidence in the over 50y age group
M>F
incidence has fallen in the west over the last 50 years - falling prevalence of h pylori and improved diet
risk factors for gastric cancer
h pylori infection cigarette smoking alcohol diet - food with nitrates/nitrite components, salt based preservatives (fresh fruit and vegetables protective!) autoimmune gastritis
presentation fo gastric cancer
history of new onset dyspepsia unintended weight loss progressive dysphagia vomiting virchow's node
main type of gastric cancer
adenocarcinoma
the two main types of gastric adenocarcinoma
intestinal-type adenocarcinomas - show gland formation, lined by mucus-secreting cells. better prognosis than diffuse type. tend to occur in older individuals
diffuse-type adenocarcinomas - consist of signet ring cells, with a diffuse pattern infiltration. very aggressive, very bad prognosis. tend to occur in younger age group.
key investigations of gastric cancer
endoscopy and biopsy
staging of gastric cancer
TNM
prognosis of gastric cancer
around 5% at 5y
gallstones epidemiology
10-15% of adult western world develop gallstones
2-4% of people with gallstones develop symptoms each year
types of gallstones
mixed stones (75%) - ca salts, bile pigment, cholesterol
cholesterol stones (20%) - large sized, yellow
bilirubinate stones (5%) - small sized, pigmented
pathogenesis of gallstones
normally cholesterol is solubilised in ice as a micelle with bile salts
an imbalance between the proportions of cholesterol and bile salts leads to precipitation of the excess component as gallstones
risk factors for cholesterol stones
female sex obesity middle age family history crohns disease
increased levels of cholesterol!
risk factors for billirubinate stones
haemolytic anaemias
investigations of gallstones
USS of gallbladder will identify 90% of gallstones
LFTs performed to assess liver function
acute cholescystitis
impacted stone occludes the cystic duct for a prolonged period of time, it will rub and damage the mucosal lining and thereby incite an acute inflammatory response in the gallbladder wall - development of acute cholecystitis
the presence of fever usually indicated acute cholecystitis
what is acute acalculus cholecystitis
thought to result from ischaemia - cystic after is an end artery
chronic cholecystitis
repeated episodes of biliary colic and acute cholecystitis result in chronic inflammation with healing by fibrosis.
as a consequence, the gallbladder wall becomes thickened and the gallbladder shrinks size
ascending cholangitis
if a gallstone impacts and obstructs the common bile duct it will cause obstructive jaundice
the jaundice develops because bile is unable to drain into the duodenum for excretion
this can develop into ascending cholangitis which is inflammation of the bile duct - biliary obstruction causes stasis which predisposes to superimposed infection: gut bacteria gain entry to the biliary tree via the ampulla of vater
what is charcot’s triad?
jaundice
fever (usually with rigors)
RUQ pain
relationship between gallstones and acute pancreatitis
if a gallstone passes down the CBD and obstructs the ampulla of water it will result in acute pancreatitis
reflux of pancreatic secretions back up the pancreatic duct which causes pancreatic auto digestion and results in pancreatitis
what is gallstone ileus
gallstone larger enough to cause small bowel obstruction enters the small bowel via a fistula which forms between the inflamed wall of the gallbladder and a loop of small bowel.
colicky abdominal pain, vomiting, distension, absolute constipation
courvoisier’s law
in a jaundiced patient, the presence of a palpable gallbladder means that the jaundice is unlikely to be due to gallstones impacted in the biliary system
This is because a patient with jaundice due to a gallstone in the common bile duct is likely to have a fibrotic shrunken gallbladder because of repeated episodes of biliary colic and acute cholecystitis As a consequence, the gallbladder is impalpable.
what are the functions of the pancreas
exocrine - secreting digestive enzymes into the pancreatic duct system
endocrine - secreting hormones such as insulin and glucagon directly into the blood
what is the most common type of pancreatic cancer
adenocarcinoma arising from the glandular duct cells that line the ducts of the exocrine system
what are the risk factors fro pancreatic cancer?
smoking is the only well recognised risk factor
occurs more in elderly males
head of pancreas presentation
obstructive jaundice
B symptoms
management of pancreatic cancer
majority (80%) present with advanced disease ad treatment is palliative - chemo, stunting CBD, symptom control
minority (20%) are suitable for curative surgery (Whipples Procedure) when tumour appears to be confined to the pancreas and lymph nodes are not involved
what is a whiles procedure?
In a Whipple’s pancreatico-duodenectomy, the distal stomach, gallbladder, common bile duct, head of pancreas, duodenum, proximal jejunum and regional lymph nodes are resected.
The reconstruction restores intestinal function by re-establishing flow of pancreatic juices, bile and food along the GI tract.
pancreatic cancer prognosis
After a Whipple’s procedure, the 5 year survival is between 20-40%.
In contrast, the overall survival for pancreatic cancer at 5 years (including the majority of patients who have advanced disease) is about 5%.
what is coeliac disease
intolerance to gluten (GLIADIN) which is found in wheat, barley and rye
pathogenesis of coeliac disease
The pathogenesis of coeliac disease is not fully understood: it is thought that gliadin triggers inappropriate
activation of intestinal T cells in genetically susceptible individuals (people with HLA-DQ2 and HLA-DQ8 haplotypes), resulting in damage to intestinal epithelial cells.
Gluten is digested by luminal and brush-border enzymes in the small intestine into amino acids and peptides, including a 33-amino acid gliadin peptide. Gliadin is deamidated (deamidation = removal of an amide group from an organic compound) in the mucosa by *ssue transglutaminases (tTG).
In individuals with the HLA-DQ2 and HLA-DQ8 haplotypes, the deamidated gliadin closely fits the MHC II grooves and is presented to T helper cells by an;gen presenting cells.
This initiates a Th2- predominant immune
response which generates cytotoxic T cells
against gliadin.
The cytotoxic T cells migrate into the intestinal
epithelium which is visible on biopsy as
intraepithelial lymphocytes [intraepithelial = within the epithelium].
The T cells damage and destroy epithelial cells resulting in progressive villous atrophy. As a result, the crypts become hyperplastic to compensate for the cell loss.
what antibodies are useful diagnostically in coeliac disease?
antigliadin
antiendomysial
antiTTG
clinical presentation of coeliac disease
malabsorption symtoms (diarrhoea, steatorrhoea, weight loss, lethargy,bloating, abdo pain)
non specific symptoms e.g. anaemia, IBS, abdo pain
failure to thrive and delayed puberty in children
dermatitis herpetiformis over elbows - itchy and blistering
some are symptomatic
diagnosis of coeliac disease
history and examination
serology: total IgA, IgA tTG, EMA
(must be eating gluten 6 weeks)
gold standard is endoscopy and duodenal biopsy
treatment of coeliac disease
life long gluten free diet
complications of coeliac disease
malabsorption
osteopenia/osteoporosis
dermatitis herpetiformis
lymphoma
clinical features of peritonitis
tachycardia pyrexia tenderness and guarding rebound tenderness localised pain during distant palpation absence of bowel sounds
investigations of peritonitis
primarily a clinical diagnosis FBC (leucocytosis) serum amylase would show pancreatitis erect CXR would show perforation CT may pinpoint the cause
management of peritonitis
IV fluids and electrolyte replacement antibiotic therapy pain relief gastric aspiration surgery may be indicated depending on the cause
types of intestinal obstruction
mechanical obstruction
paralytic obstruction
how can mechanical obstruction be classified
speed of onset
anatomical site
simple vs strangulating
open loop vs closed loop
causes of small bowel obstruction
- ADHESIONS
- hernias
interssusception
volvulus
crohn’s disease
causes of large bowel obstruction
colorectal cancer (adenocarcinoma)
diverticular strictures
sigmoid volvulus
what is intussusception?
when a segment of small bowel prolapses into the immediately adjoining bowel
commonest form is ileocolic
what is volvulus
abnormal twisting of a segment of the bowel around its site of a mesenteric attachment resulting in a closed loop obstruction
there is also occlusion of the main vessels at the base of the involved mesentery which amy result in strangulation
most commonly occurs in the SIGMOID, but can also occur in the caecum and small intestine
what are precipitating factors of volvulus?
abnormally mobile loop of intestine e.g. a particularly long sigmoid loop
abnormally loaded loop e.g. chronic constipation
loop fixed at its base by adhesions, around which it rotates
a loop of bowel with a narrow mesenteric attachment
management of volvulus
Volvulus may be treated by passing a long soft rectal tube through a sigmoidoscope and advancing it into the sigmoid colon. This often untwists an early volvulus and is accompanied by passage of vast amounts of flatus and liquid faeces. If this fails, the volvulus is untwisted at laparotomy and the bowel is decompressed via a rectal tube threaded up from the anus. If infarcMon/gangrene has occurred, the affected segment is resected and the two open ends are brought out as a double-barreled colostomy which is later closed.
Colorectal cancer and obstruction
• bowel cancer (almost always adenocarcinoma) may present as large bowel obstruction. This is more
common with left-sided tumours because the bowel contents are more solid by the Mme they reach the
left side.
• the obstruction may be chronic with insidious onset and slowly progressive symptoms. A chronic
obstruction may develop acute symptoms as the obstruction suddenly becomes complete (ie. when a
narrowed lumen becomes totally occluded). This is often termed acute-on-chronic obstruction.
• don’t forget that colorectal cancer presents as an emergency (such as bowel obstruction) in around 20%
of cases.
common causes of bowel obstruction in neonates
congenital atresia and stenosis
volvulus
hirschsprung’s disease
meconium ileus
common causes of bowel obstruction in infants
intussusception
hirschsprung’s disease
strangulated hernia
mocker’s diverticulum
clinical features of mechanical bowel obstruction
colicky abdo pain
abdo distension
vomiting
absolute constipation
changed bowel sounds (tinkling eventually) dehydration hypotension tachycardia empty rectum on PR examination
signs of strangulating obstruction
toxic appearance with tachycardia and fever
colicky pain becoming continuous as peritonitis develops
tenderness, guarding rebound tenderness
absent bowel sounds
management of mechanical bowel obstruction
iv fluid/electrolytes close monitoring NG suction (drip and suck) iv antibiotics if strangulation is suspected investigate the cause
causes of paralytic ileus
postoperative state
generalised peritonitis
drugs e.g. opiates, anticholinergics
electrolyte imbalances
pathophysiology of paralytic ileus
The effects of paralytic ileus are similar to those of a simple mechanical obstruction:
The lack of coordinated peristalsis results in a functional obstruction. Gas (mainly swallowed air) and fluid/ electrolytes accumulate in the bowel lumen. As the bowel dilates, the blood supply to the bowel is compromised resulting in ischaemia which, if not reversed, may result in infarction (gangrene) and perforation.
clinical features of paralytic ileus
pain - but NOT colicky
abdo distention
constipation
ileus
causes of bowel infarction
strangulating bowel obstruction embolus causing obstruction of a mesenteric artery thrombus occlusion aortic dissection into mesenteric artery compression of veins in bowel wall vasculitis
clinical features of bowel infarction
colicky abdo pain
rectal bleeding
shock
elderly with AF
may produce similar signs to peritonitis
management of bowel infarction
The management of bowel infarction is beyond the scope of these notes. However, in general the patient should be resuscitated with iv fluids and given broad spectrum antibiotocs. They usually undergo urgent laparotomy where any dead bowel is resected. Revascularisation by embolectomy or bypass may improve doubkully viable bowel and allow primary anastomosis.
where sis the most common site of diverticular disease
sigmoid
what is a diverticulum
a pouch of colonic mucosa that has herniated through the muscularis propria and has come to lie in the subserosal (pericolic) fat outside the bowel wall
important factors in the development of diverticula
areas of weakness in the colonic wall
raised intraluminal pressure due to insufficient dietary fibre
diverticulosis
diverticula are present but asymptomatic
diverticulitis
acutely inflamed diverticulum. this is the most common presentation
acute diverticulitis
initiated when faecal matter impacts and obstructs the neck of a diverticulum
this traps bacteria with consequence bacterial replication in the occluded lumen resulting in infection and mucosal injury
local trauma (rubbing) to the mucosa by the faecolith may also cause mucosal injury
complications of diverticular disease
abscess formation perforation and peritonitis fistula stricture lower GI bleeding
management of peptic ulcers
triple therapy: 2x ABx and PPI
amoxicillin and clarythromycin
lanzoprazole, omeprazole
causes of acute pancreatitis
IGETSMASHED
idiopathic gallstones ethanol trauma steroids mumps autoimmune scorpion venom hypothermia/hypercalcaemia/hyperlipidaemia ERCP and emboli drugs
pancreatitis investigations
amylase and LIPASE ABG AXR CT USS ERCP CRP
complications of pancreatitis
abscess shock renal failure sepsis bleeding thrombosis
fistulae
management of pancreatitis
severity assessment (glasgow criteria - PANCREAS)
NBM, NJ tube, fluids
analgesia
hourly and daily monitoring
possible ITU, oxygen, ABx
ERCP and gallstone removal is progressive jaundice
repeat imaging to monitor
glasgow criteria for severity pancreatitis
PaO2 <8kPa Age >55y Neutrphilia >15 Calcium <2 Renal function (urea >16) Enzyme (LDH <600, AST <200) Albumin <32 Sugar >10
C diff infection signs and symptoms
foul odour of stool, green brown
significant diarrhoea
fever
abdominal pain
management of acute liver failure
ABCDE vitamin K if PTT is raised stop all hepatotoxic drugs Abx prophylaxis if ascites to stop SBP daily bloods lactulose - helps remove ammonia close monitoring
examples of hepatotoxic drugs
paracetamol
rifampicin
pyrazinamide
common causes of upper GI bleeds
varices 10-20% reflux oesophagitis 2-5% mallory-weiss 5-10% peptic ulcers 50% haemorrhage gastropathy and erosions 15-20% drugs malignancy
treatment of bleeding oesophageal varices
banding, sclerotherapy, sengstaken-blakemore tube
treatment of peptic ulcers
endoscopic haemostats with adrenaline injection, coagulation with thermal therapy, IV PPI therapy for 72 hours following endoscopic therapy
Acute hepatitis symptoms and stages
- prodromal stage - non specific flu like symptoms
- yellowing of the skin and eyes (up to 4 weeks) - hepatomegaly, abdo pain, ?splenomegaly, weight loss
- recovery phase - resolution of symptoms, but still increased LFTs and hepatomegaly
Ulcerative Collitis
diarrhoea, often with blood
relapses and remits
severe fulminant colitis
LIF pain
only colon, begins in rectum and extends proximally
continuous
red mucosa, bleeds easily
mucosal inflammation
goblet cell depletion and crypt abscesses
Crohn’s disease
abdominal pain weight loss RIF pain diarrhoea bleeding anal tags, fissures, etc relapses and remits
all of GIT oral and perianal skip lesions cobblestone appearance transmural inflammation granulomas in 50%
management of IBD
oral 5-ASA mesalazine steroids: prednisolone, IV hydrocortisone liquid internal nutrition thiopurine drugs metronidazole methotrexate
colectomy or panproctocolectomy are surgical options if medication failure or complications
extra-gut manifestations of IBD
eyes - uveitis, conjunctivitis
joints - arthralgia, arthritis
skin - erythema nodosum, pyoderma gangrenous
hepatobiliary - fatty liver, sclerosing cholangitis, chronic hepatitis, cirrhosis, gallstone
renal calculi - oxalate stones
complications of IBD
toxic dilation of colon and perforation stricture formation abscess formation (CD) fistulae and issues (CD) colon cancer
