Pathology Flashcards
what happens when acid enters the oesophagus?
- thickening of squamous epithelium
- ulceration
complications of oesophageal reflux
- healing by fibrosis
- barrett’s oesophagus
what occurs in healing by fibrosis
- stricture formation
- impaired oesophageal motility
- oesophageal obstruction
what transformation occurs in barrette oesophagus?
squamous epithelium -> glandular epithelium
what is primary influence on rising rates of oesophageal cancer?
environmental factors e.g. smoking
two histological types of oesophageal cancer
- squamous carcinoma
- adenocarcinoma (developed from Barretts oesophagus
risk factors for oesophageal cancer - squamous carcinoma
smoking
alcohol
dietary carcinogens
risk factors for oesophageal cancer adenocarcinoma
barretts metaplasia
obesity
why does obesity influence rates of oesophageal cancer
because intrabdominal pressure is increased, increasing rate of reflux
local effects of oesophageal cancer
obstruction
ulceration
perforation
methods of spread of oesophageal cancer
- direct (to surrounding structures)
- lymphatic spread (to regional lymph nodes)
- blood spread (liver)
prognosis oesophageal cancer
5 year survival <15%
pathology (causes/types) of gastritis
Type A - Autoimmune
Type B - Bacterial
Type C - Chemical Injury
describe Autoimmune gastritis
- organ specific autoimmune disease
- autoantibodies to parietal cells and intrinsic factor
what should be considered when a diagnosis of autoimmune gastritis is made?
that it can be associated with other automimmune diseases in different locations throughout the body
pathology of autoimmune gastritis (what happens in it)
- atrophy of specialised acid secreting gastric epithelium
- loss of specialised gastric epithelial cells
result of pathology for autoimmune gastritis
- decreased acid secretion
- loss of intrinsic factor (vitamin B12 deficiency)
what is the commonest type of gastritis
bacterial gastritis
what type of bacteria most commonly causes bacterial gastritis
helicobacter pylori
helicobacter pylori
- gram negative bacteria
- found in gastric mucus on surface of gastric epithelium
- produces acute and chronic inflammatory response
- increased acid production
what can cause chemical gastritis
- drugs (NSAIDS)
- alcohol
- bile reflux
what is peptic ulceration
inbalance between acid secretion and mucosal barrier
where does peptic ulceration occur>
- lower oesophagus
- body and antrum of stomach
- first and second parts of duodenum
what organism is usually associated with chemical gastritis
H. Pylori (increases gastric acid production)
complications of peptic ulceration
- bleeding
- perforation
- healing by fibrosis
what can occur as a result of peritonitis as a complication of peptic ulceration
perforation: erosion through all layers of the stomach
pathology of gastric cancer
- develops through phases of intestinal metaplasia and dysplasia
- H.Pylori
metaplasia
reversible transformation of one differentiated cell type to another differentiated cell type
dysplasia
abnormality of development or an epithelial anomaly of growth and differentiation
histology of gastric cancer
adenocarcinoma
where do adenocarcinomas arise from
glandular structures in epithelial tissue
routes of spread of stomach cancer
- direct
- lymphatic
- blood
- transcoelomic
describe transcoelomic spread of stomach cancer
- spread within peritoneal cavity
- if the cancer goes through all the layers of the stomach wall, it can spread from the outside surface and metastasis around the peritoneal cavity
prognosis of stomach cancer
5 year survival <20%
pathway of bilirubin metabolism
- pre hepatic
- hepatic
- post hepatic
what is involved in the pre hepatic stage of bilirubin metabolism
- breakdown of haemoglobin -> haem converted to bilirubin -> bilirubin released into circulation
what is involved in hepatic stage of bilirubin metabolism
- uptake of bilirubin by hepatocytes
- conjugation of bilirubin in hepatocytes
- excretion of conjugated bilirubin into binary system
what is involved in post-hepatic stage of bilirubin metabolism
- transport of conjugated bilirubin in biliary system
- breakdown of bilirubin conjugate in intestine
- re-absorption of bilirubin into circulatory system
classifications of causes of jaundice
pre-hepatic
hepatic
post-hepatic
bile canaliculi location
very small structures found immediately adjacent to hepatocytes
bile canaliculi definition and function
thin tubes that collect bile secreted by hepatocytes
difference between predictable and unpredictable cholestasis
predictable = dose related
unpredictable = not dose related
hepatic causes of jaundice
cholestasis
intra-hepatic bile duct obstruction
three types of tumours of the liver causing intra hepatic bile obstruction
- hepatocellular carcinoma
- tumours of intra-hepatic bile ducts
- metastatic tumours
differences between different tumours of the liver causing intrahepatic bile duct obstruction
hepatocellular carcinomas and tumours of intra-hepatic bile ducts are normally just one tumour, whereas metastatic tumours are normally multiple
cryptogenic
unknown cause
types of cells in the small bowl
goblet cells
columnar absorptive cells
endocrine cells
how often are small bowl cells renewed
every 4-6 days
describe the histology of the large bowl
- flat
- no villi
- tubular crypts
- surface-columnar absorptive cells
- crypts (goblet cells, endocrine cells, stem cells)
how often large bowl cells renewed
every 3-8 days
What is small and large bowl peristalsis mediated by?
- intrinsic (myenteric plexus)
- extrinsic (autonomic innervation)
location of Meisseners plexus
base of submucosa
location of Auerbach plexus
between inner circular and outer longitudinal layers of muscularis propria
define idiopathic inflammatory bowl disease
chronic inflammatory conditions resulting from inappropriate and persistent activation of the mucosal immune system driven by the presence of normal intraluminal flora
dysplasia
he presence of cells of an abnormal type within a tissue
what would you see in a histolological sample of chronic ischaemia
mucosal inflammation
ulceration
submucosal inflammation
fibrosis
stricture
what would you see in a histolological sample of acute ischaemia
oedema
interstitiial haemorrhages
sloughing necrosis, ghost outlines of cells
nuclei indistinct
initial absence of inflammation
1-4 days - bacteria, gangrene and perforation
vascular dilation
histology of radiation colitis
- bizarre cellular changes
- inflammation
- crypt abscesses
- eosinophils
- later-arterial stenosis
- ulceration
- necrosis
- haemorrhages
- perforation
histology of appendicitis
inflammation in appendix wall
pus in lumen
acute gangrenous - full thickness necrosis +/- perforation
which colorectal adenocarcinoma is more likely to present later and why
right sided due to the liquid state of the faeces. this means it can squeeze past any bulges, polyps easier
