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MCD Cell Pathology > 6 Case Studies > Flashcards

6 Case Studies Flashcards

1
Q

Q: What is Helicobacter pylori? Tendancy?

A

A: common type of bacteria that grows in the digestive tract and has a tendency to attack the stomach lining

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2
Q

Q: What percentage of people have H. pylori and are asymptomatic?

A

A: 80%

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3
Q

Q: What are the 3 main effects of H. pylori on the stomach?

A

A: -inflammation: acute, chronic (including ulcers)

  • cell damage: atrophy, metaplasia, dysplasia
  • neoplasia: 2 types being carcinoma and lymphoma
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4
Q

Q: What are the main causes of gatritis? (3)

A

A: -chemical agents (drugs)

  • infectious agents (H pylori)
  • immunological reactions (autoimmune)
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5
Q

Q: What is gastritis?

A

A: inflammation of the lining of the stomach

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6
Q

Q: What are ulcers? caused by?

A

A: open sore on an external or internal body surface caused by break in skin or mucous membrane which fails to heal

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7
Q

Q: What are the 4 clinical outcomes of H pylori infections?

A

A: 1. asymptomatic

  1. chronic atrophic gastritis (intestinal metaplasia and inflammation and damage)
  2. gastric or duedemal ulcer
  3. gastric cancer / MALT lymphoma
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8
Q

Q: How does a normal stomach look? (endoscopy) (2)

A

A: rugel folds and light pink colour

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9
Q

Q: How does a stomach with acute gastritis look? (endoscopy) (3)

A

A: redness, swelling (and pain)

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10
Q

Q: What’s the key inflammatory cell of acute inflammation?

A

A: neutrophil polymorph

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11
Q

Q: Describe an abscess. (2)

A

A: lots of dead and decaying neutrophils associated with dead and dying tissue

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12
Q

Q: How does a stomach with chronic gastritis look? (endoscopy) (2)

A

A: atrophy seen

loss of many cells= looks flat

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13
Q

Q: What’s the key inflammatory cell of chronic inflammation?

A

A: lymphocyte

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14
Q

Q: How does a stomach with chronic gastritis look? (histology) Where is this normally seen?

A

A: lymphode follicles/pale germinal centres -> normally seen in lymph nodes and not seen in normal stomach

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15
Q

Q: What is granulomatous inflammation? showing? (2) Involves?

A

A: particular form of chronic inflammation showing:

  • granuloma formation
  • cluster of macrophages
  • involves specific immune reaction T cells
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16
Q

Q: What causes granulomers in the stomach? What is a granulomer?

A

A: heliocobacter

organised collection of epithelium macrophages that have been activated for secretion rather that phagocytosis

17
Q

Q: What are the causes of granulomatous inflammation? (4)

A

A: -infection, TB, fungi, heliocobacter

  • foreign material
  • reaction to tumours
  • immune diseases (sarcoid, Chron’s)
18
Q

Q: What’s the difference between acute and chronic ulcers?

A

A: chronic have scarring (fibrosis)

19
Q

Q: What are the 2 outcomes of wound (ulcer) healing?

A

A: -parenchymal cell regeneration and RESOLUTION = acute gastric ulcer

-REPAIR by connective tissue and SCAR TISSUE FORMATION = chronic gastric ulcer

20
Q

Q: Name 3 cellular adaptations seen in association with heliobacter gastritis.

A

A: atrophy, metaplasia, dysplasia

21
Q

Q: Explain why dysplasia means that heliobacter gastritis can be cured by local treatment.

A

A: dysplasia means no invasion of underlying tissue -> means not spreading

22
Q

Q: Describe heliobacter gastritis metaplasia.

A

A: gastric to intestinal cells

23
Q

Q: How are neoplasms classified? (2)

A

A: according to cell of origin and if they’re benign or malignant

24
Q

Q: What are lymphomas? What can cause them? what else can this cause?

A

A: malignant tumour of lymphoid tissue

associated with helicobacter gastritis

HELICOBACTER CAN CAUSE ADENOCARCINOMAS and LYMPHOMAS

25
Q

Q: What is the main staging system?

A

A: TNM is the main staging system (different TNM for each organ)

26
Q

Q: Name 3 common sites for clinically important atheroma. Include 2 risks associated with 2 sites.

A

A: coronary arteries (risk of myocardial infarction)

carotid arteries (risk of stroke)

aorta and / or iliac arteries

27
Q

Q: What is an atheroma? caused by?

A

A: degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue

28
Q

Q: How can arterial walls be weakened and lead to an aneurysm formation? (5) What is the aneurysm?

A

A: Thick atheromatous plaque in the intima reduces the diffusion of nutrients from inside the wall

Nutrition of the wall is depressed and you get atrophy of the muscle fibres

Muscle fibres are replaced by fibrous tissue

aneurysm= bulge where weakened wall is

29
Q

Q: What can myocardial fibrosis lead to? (2) What does it look like?

A

A: chronic cardiac failure and sudden death (within 24hrs)

heart has white patched

30
Q

Q: What can stable atherosclerotic plaques lead to? (3)

A

A: -stable angina

  • dementia
  • chronic lower limb ischaemia
31
Q

Q: What can thrombosis overlying an unstable atherosclerotic plaque lead to? (4)

A

A: -unstable angina

  • myocardial infarction
  • cerebral infarction
  • acute lower limb ischaemia
32
Q

Q: Compare infarction and ischaemia.

A

A: Ischemia refers to reduction in blood supply to an organ. If ischaemia is reversed rapidly there is no permanent damage to the organ. Prolonged ischemia can cause necrosis of the organ tissue which is called an infarct

33
Q

Q: What details does a death certificate include?

A

A: 1a immediate cause of death

1b predisposing factor

1c predisposing factor

2 other factors contributing to but not directly leading to death

34
Q

Q: What’s an aneurysm?

A

A: weakening of an artery wall that creates a bulge, or distention, of the artery

MCD Cell Pathology (6 decks)

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