Pathology - GI Flashcards
What are the causes of chronic gastritis
h pylori
chronic bile reflux
nsaid
autoimmune
allergic response
radiation
stress
coffee, alcohol
Describe the features and complications of h pylori induced chronic gastritis
-predominantly antral and characterised by increased acid production
-bacteria secretes urease which generates ammonia (used to detect presence)
-bacteria makes phospholipases that damage surface of epithelial cells, disrupting normal mucosal defense mechanisms
complications: peptic ulcer disease, bleeding, perforation, obstruction, gastric adenocarcinoma, gastric lymphoma
By what mechanisms may h pylori cause peptic ulcers
-secretion of urease which generates ammonia that increases pH
-production of phospholipase that directly damages epithelial cell surface
-enhancement of gastric acid secretion
-h pylori proteins are immunogenic and evoke a strong inflammatory response
What complications may arise from peptic ulcer disease
-bleeding = 25% of ulcer deaths, most common complication
-perforation = 5% of patients, rarely first indication of an ulcer
-obstruction = 2% of patients, from edema and scarring
What are the pathological features and complications of crohns disease
-transmural inflammation occurring anywhere in the GI tract
-skip lesions are sharply delineated disease areas with sparing of interspersed mucosa
-non-caseating granulomas and fibrotic strictures and fistulas may be present
complications: strictures, fistulas, malabsorption syndrome, extra-intestinal manifestations, neoplasia (adenocarcinoma)
What are the extra-intestinal manifestations of crohns disease
migrating polyarthritis
sacroiliitis
ankylosing spondylosis
erythema nodosum
uveitis
cholangitis
What are the pathological features of ulcerative colitis
-ulcerating inflammation extending only into mucosa and superficial submucosa
-limited to colon and rectum, does not involve small bowel, no skip lesions
-ulcers are superficial and broad based, no fistulas
-inflammatory pseudopolyps and crypt abscesses are present, no granulomas
Extra-intestinal manifestations of ulcerative colitis and Complications
extra-intestinal manifestations: same as crohns disease, more common in ulcerative colitis
complications: toxic megacolon, primary sclerosing cholangitis, neoplasia
What are the common causes of bowel obstruction
adhesion
hernia
malignancy
volvulus, intussusception
mesenteric infarct
strictures
How does a hernia form and cause a bowel obstruction and describe the important clinical sequelae of ongoing obstruction
-weakness or defect in the abdominal wall allows for protrusion of serosa lined pouch of peritoneum (hernia sac)
-viscera (small bowl, large bowel, omentum) may then protrude through the area of weakness
-viscera may get entrapped in the hernia sac if narrow necked
-ongoing obstruction leads to venous stasis and edema, leading to incarceration and strangulation and ischaemia
complications: perforation, ischaemia, sepsis, abscess, electrolyte disturbance, death
What conditions can lead to infarction of bowel
1) Occlusive ischaemia:
-arterial thombosis = atherosclerosis, vasculitis, aortic dissection, OCP
-arterial embolism = endocarditis, aortic thromboembolism
-mesenteric venous thrombosis = hypercoagulation state, OCP, post operation
-mechanical = volvulus, stricture
2) Non-occlusive ischaemia:
-shock, cardiac failure, dehydration
What parts of the bowel are most susceptible to ischaemic injury
-watershed zones are areas located at the end of arterial supply = splenic flexure, sigmoid colon, rectum
-villi are more at risk than crypts
Describe the intestinal response to an acute ischaemic insult
1) initial hypoxic injury
-at onset of vascular compromise, epithelial cells lining intestine are relatively resistant
2) reperfusion injury
-initiated by restoration of blood supply, due to leakage of gut lumen bacterial products into systemic circulation
-characterised by free radical production and neutrophil infiltration
Describe the morphology of acute ischaemic bowel injury
-initial congestion, followed by edema and haemorrhage in wall
-lumen contains bloody fluid
-coagulative necrosis of muscularis propria occurs in 1-4 days, during which time perforation may occur
-neutrophils present at time of reperfusion
-bacterial superinfection
-metabolic and cardiovascular derangement
What are the clinical features and outcomes of ischaemic bowel
clinical: severe pain, tenderness, peritonism, nausea, vomiting, bloody diarrhoea, shock, sepsis
outcomes: strictures, segmental patchy mucosal degeneration, death
What are the common causes of infective gastroenteritis
-viral: rotavirus (most common cause of diarrhoea in children), adenovirus, norovirus
-bacterial:
ingestion of preformed toxin = staph aureus, cholera
ingestion of toxigenic organism that proliferates in lumen and forms enterotoxin = enterotoxic e coli, vibrio cholerae
infection by enteroinvasive oragnisms = shigella, salmonella
-parasites: giardia lamblia, entamoeba histolytica
What is the difference between endotoxin and exotoxin
-endotoxin: LPS in outer membrane of gram negative bacteria, cause injury via the host immune response
-exotoxin: proteins secreted by bacteria that cause direct injury
What is the causative organism of cholera and describe the pathogenesis
-cholera is caused by vibrio cholerae, a gram negative bacteria, non-invasive, has flagella proteins for attachment
-transmitted by drinking contaminated water and causes secretory diarrhoea (rice water)
-vibrio does not enter epithelia cells itself, but produces a pre-formed cholera enterotoxin:
1) B subunit binds to intestinal epithelial cells
2) A subunit transfer to cytoplasm, act on G protein, cause CFTR to open and Cl- secretion into lumen and massive water shift
What bacterial class does escherichia coli belong to and what types of infections can they cause
-e coli is a gram negative rod, facultative anaerobe, normal GI pathogen
infections: UTI, prostatitis, epididymo-orchitis, infectious enterocolitis, cholecystitis, bacterial peritonitis
List the e coli enteritis types and describe their features
-ETEC = enterotoxic, produce a toxin, causes travellers diarrhoea
-EPEC = enteropathogenic, causes endemic diarrhoea
-EHEC = enterohaemorrhagic, produces a shigella like toxin, causes bloody diarrhoea
-EIEC = enteroinvasive, not toxin producing, invades epithelial cells and causes colitis
-EAEC = enteroaggregative, produce shigella like toxin, cause non-bloody diarrhoea
What is pseudomembranous colitis, the risk factors for developing and the clinical features
-formation of pseudomembrane (adherent layer of inflammatory cells and debris) overlying mucosal injury
-associated with antibiotic use causing disruption of normal flora and overgrowth of bacteria
-epithelial denudation, lamina propria with infiltrate of neutrophils and damaged crypts coalesce to form pseudomembrane
-caused by c diff, salmonella, c perfringens and staph aureus
risks: advanced age, hospitalisation, antibiotic treatment
clinical: fever, leukocytosis, abdominal pain, watery diarrhoea
What are the c diff toxins
Toxin A = stimulates chemokine production and recruitment of leukocytes
Toxin B = causes cytopathic effects and is used to diagnose c diff
What type of bacteria is salmonella and describe the pathogenesis and clinical features of typhoid fever
-gram negative bacillus, flagellated, food and water born, cause typhoid fever and non-typhoid fever infections
-typhoid fever pathogenesis: cause by salmonella typhi and paratyphi
travel in India, Mexico, Phillipines, Pakistan, humans only reservoir, transmission through contaminated food and water
organisms are resistant to gastric acid and invade M cells and disseminate via lymphatics and blood vessels
infection causes expansion of Peyers patches and draining nodes, liver shows typhoid nodules
-typhoid fever clinical: initial dysentery followed by bacteraemia, fevers, abdominal pain
What is the causative organism and pathogenesis of salmonella dysentery
cause: salmonella enteritidis and typhimurium
pathogenesis: invades epithelium, taken up by macrophages, gut wall inflammation, neural reflex pathway
