Pathology Flashcards

1
Q

what happens when acid enters the oesophagus?

A
  • thickening of squamous epithelium

- ulceration

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2
Q

complications of oesophageal reflux

A
  • healing by fibrosis

- barrett’s oesophagus

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3
Q

what occurs in healing by fibrosis

A
  • stricture formation
  • impaired oesophageal motility
  • oesophageal obstruction
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4
Q

what transformation occurs in barrette oesophagus?

A

squamous epithelium -> glandular epithelium

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5
Q

what is primary influence on rising rates of oesophageal cancer?

A

environmental factors e.g. smoking

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6
Q

two histological types of oesophageal cancer

A
  • squamous carcinoma

- adenocarcinoma (developed from Barretts oesophagus

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7
Q

risk factors for oesophageal cancer - squamous carcinoma

A

smoking
alcohol
dietary carcinogens

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8
Q

risk factors for oesophageal cancer adenocarcinoma

A

barretts metaplasia

obesity

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9
Q

why does obesity influence rates of oesophageal cancer

A

because intrabdominal pressure is increased, increasing rate of reflux

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10
Q

local effects of oesophageal cancer

A

obstruction
ulceration
perforation

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11
Q

methods of spread of oesophageal cancer

A
  • direct (to surrounding structures)
  • lymphatic spread (to regional lymph nodes)
  • blood spread (liver)
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12
Q

prognosis oesophageal cancer

A

5 year survival <15%

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13
Q

pathology (causes/types) of gastritis

A

Type A - Autoimmune
Type B - Bacterial
Type C - Chemical Injury

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14
Q

describe Autoimmune gastritis

A
  • organ specific autoimmune disease

- autoantibodies to parietal cells and intrinsic factor

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15
Q

what should be considered when a diagnosis of autoimmune gastritis is made?

A

that it can be associated with other automimmune diseases in different locations throughout the body

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16
Q

pathology of autoimmune gastritis (what happens in it)

A
  • atrophy of specialised acid secreting gastric epithelium

- loss of specialised gastric epithelial cells

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17
Q

result of pathology for autoimmune gastritis

A
  • decreased acid secretion

- loss of intrinsic factor (vitamin B12 deficiency)

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18
Q

what is the commonest type of gastritis

A

bacterial gastritis

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19
Q

what type of bacteria most commonly causes bacterial gastritis

A

helicobacter pylori

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20
Q

helicobacter pylori

A
  • gram negative bacteria
  • found in gastric mucus on surface of gastric epithelium
  • produces acute and chronic inflammatory response
  • increased acid production
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21
Q

what can cause chemical gastritis

A
  • drugs (NSAIDS)
  • alcohol
  • bile reflux
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22
Q

what is peptic ulceration

A

inbalance between acid secretion and mucosal barrier

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23
Q

where does peptic ulceration occur>

A
  • lower oesophagus
  • body and antrum of stomach
  • first and second parts of duodenum
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24
Q

what organism is usually associated with chemical gastritis

A

H. Pylori (increases gastric acid production)

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25
complications of peptic ulceration
- bleeding - perforation - healing by fibrosis
26
what can occur as a result of peritonitis as a complication of peptic ulceration
perforation: erosion through all layers of the stomach
27
pathology of gastric cancer
- develops through phases of intestinal metaplasia and dysplasia - H.Pylori
28
metaplasia
reversible transformation of one differentiated cell type to another differentiated cell type
29
dysplasia
abnormality of development or an epithelial anomaly of growth and differentiation
30
histology of gastric cancer
adenocarcinoma
31
where do adenocarcinomas arise from
glandular structures in epithelial tissue
32
routes of spread of stomach cancer
- direct - lymphatic - blood - transcoelomic
33
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
34
prognosis of stomach cancer
5 year survival <20%
35
pathway of bilirubin metabolism
1. pre hepatic 2. hepatic 3. post hepatic
36
what is involved in the pre hepatic stage of bilirubin metabolism
- breakdown of haemoglobin -> haem converted to bilirubin -> bilirubin released into circulation
37
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
38
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
39
classifications of causes of jaundice
pre-hepatic hepatic post-hepatic
40
bile canaliculi location
very small structures found immediately adjacent to hepatocytes
41
bile canaliculi definition and function
thin tubes that collect bile secreted by hepatocytes
42
difference between predictable and unpredictable cholestasis
predictable = dose related unpredictable = not dose related
43
hepatic causes of jaundice
cholestasis intra-hepatic bile duct obstruction
44
three types of tumours of the liver causing intra hepatic bile obstruction
1. hepatocellular carcinoma 2. tumours of intra-hepatic bile ducts 3. metastatic tumours
45
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
46
cryptogenic
unknown cause
47
types of cells in the small bowl
goblet cells columnar absorptive cells endocrine cells
48
how often are small bowl cells renewed
every 4-6 days
49
describe the histology of the large bowl
- flat - no villi - tubular crypts - surface-columnar absorptive cells - crypts (goblet cells, endocrine cells, stem cells)
50
how often large bowl cells renewed
every 3-8 days
51
What is small and large bowl peristalsis mediated by?
- intrinsic (myenteric plexus) | - extrinsic (autonomic innervation)
52
location of Meisseners plexus
base of submucosa
53
location of Auerbach plexus
between inner circular and outer longitudinal layers of muscularis propria
54
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
55
dysplasia
he presence of cells of an abnormal type within a tissue
56
what would you see in a histolological sample of chronic ischaemia
mucosal inflammation ulceration submucosal inflammation fibrosis stricture
57
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
58
histology of radiation colitis
- bizarre cellular changes - inflammation - crypt abscesses - eosinophils - later-arterial stenosis - ulceration - necrosis - haemorrhages - perforation
59
histology of appendicitis
inflammation in appendix wall pus in lumen acute gangrenous - full thickness necrosis +/- perforation
60
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