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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
Q

complications of peptic ulceration

A
  • bleeding
  • perforation
  • healing by fibrosis
26
Q

what can occur as a result of peritonitis as a complication of peptic ulceration

A

perforation: erosion through all layers of the stomach

27
Q

pathology of gastric cancer

A
  • develops through phases of intestinal metaplasia and dysplasia
  • H.Pylori
28
Q

metaplasia

A

reversible transformation of one differentiated cell type to another differentiated cell type

29
Q

dysplasia

A

abnormality of development or an epithelial anomaly of growth and differentiation

30
Q

histology of gastric cancer

A

adenocarcinoma

31
Q

where do adenocarcinomas arise from

A

glandular structures in epithelial tissue

32
Q

routes of spread of stomach cancer

A
  • direct
  • lymphatic
  • blood
  • transcoelomic
33
Q

describe transcoelomic spread of stomach cancer

A
  • 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
Q

prognosis of stomach cancer

A

5 year survival <20%

35
Q

pathway of bilirubin metabolism

A
  1. pre hepatic
  2. hepatic
  3. post hepatic
36
Q

what is involved in the pre hepatic stage of bilirubin metabolism

A
  • breakdown of haemoglobin -> haem converted to bilirubin -> bilirubin released into circulation
37
Q

what is involved in hepatic stage of bilirubin metabolism

A
  • uptake of bilirubin by hepatocytes
  • conjugation of bilirubin in hepatocytes
  • excretion of conjugated bilirubin into binary system
38
Q

what is involved in post-hepatic stage of bilirubin metabolism

A
  • transport of conjugated bilirubin in biliary system
  • breakdown of bilirubin conjugate in intestine
  • re-absorption of bilirubin into circulatory system
39
Q

classifications of causes of jaundice

A

pre-hepatic
hepatic
post-hepatic

40
Q

bile canaliculi location

A

very small structures found immediately adjacent to hepatocytes

41
Q

bile canaliculi definition and function

A

thin tubes that collect bile secreted by hepatocytes

42
Q

difference between predictable and unpredictable cholestasis

A

predictable = dose related

unpredictable = not dose related

43
Q

hepatic causes of jaundice

A

cholestasis

intra-hepatic bile duct obstruction

44
Q

three types of tumours of the liver causing intra hepatic bile obstruction

A
  1. hepatocellular carcinoma
  2. tumours of intra-hepatic bile ducts
  3. metastatic tumours
45
Q

differences between different tumours of the liver causing intrahepatic bile duct obstruction

A

hepatocellular carcinomas and tumours of intra-hepatic bile ducts are normally just one tumour, whereas metastatic tumours are normally multiple

46
Q

cryptogenic

A

unknown cause

47
Q

types of cells in the small bowl

A

goblet cells

columnar absorptive cells

endocrine cells

48
Q

how often are small bowl cells renewed

A

every 4-6 days

49
Q

describe the histology of the large bowl

A
  • flat
  • no villi
  • tubular crypts
  • surface-columnar absorptive cells
  • crypts (goblet cells, endocrine cells, stem cells)
50
Q

how often large bowl cells renewed

A

every 3-8 days

51
Q

What is small and large bowl peristalsis mediated by?

A
  • intrinsic (myenteric plexus)

- extrinsic (autonomic innervation)

52
Q

location of Meisseners plexus

A

base of submucosa

53
Q

location of Auerbach plexus

A

between inner circular and outer longitudinal layers of muscularis propria

54
Q

define idiopathic inflammatory bowl disease

A

chronic inflammatory conditions resulting from inappropriate and persistent activation of the mucosal immune system driven by the presence of normal intraluminal flora

55
Q

dysplasia

A

he presence of cells of an abnormal type within a tissue

56
Q

what would you see in a histolological sample of chronic ischaemia

A

mucosal inflammation

ulceration

submucosal inflammation

fibrosis

stricture

57
Q

what would you see in a histolological sample of acute ischaemia

A

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
Q

histology of radiation colitis

A
  • bizarre cellular changes
  • inflammation
  • crypt abscesses
  • eosinophils
  • later-arterial stenosis
  • ulceration
  • necrosis
  • haemorrhages
  • perforation
59
Q

histology of appendicitis

A

inflammation in appendix wall

pus in lumen

acute gangrenous - full thickness necrosis +/- perforation

60
Q

which colorectal adenocarcinoma is more likely to present later and why

A

right sided due to the liquid state of the faeces. this means it can squeeze past any bulges, polyps easier

GI (35 decks)

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