6 Case Studies

Question 1

Q: What is Helicobacter pylori? Tendancy?

Answer 1

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

Question 2

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

Answer 2

A: 80%

Question 3

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

Answer 3

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

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

Question 4

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

Answer 4

A: -chemical agents (drugs)

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

Question 5

Q: What is gastritis?

Answer 5

A: inflammation of the lining of the stomach

Question 6

Q: What are ulcers? caused by?

Answer 6

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

Question 7

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

Answer 7

A: 1. asymptomatic

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

Question 8

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

Answer 8

A: rugel folds and light pink colour

Question 9

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

Answer 9

A: redness, swelling (and pain)

Question 10

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

Answer 10

A: neutrophil polymorph

Question 11

Q: Describe an abscess. (2)

Answer 11

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

Question 12

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

Answer 12

A: atrophy seen

loss of many cells= looks flat

Question 13

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

Answer 13

A: lymphocyte

Question 14

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

Answer 14

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

Question 15

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

Answer 15

A: particular form of chronic inflammation showing:

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

Question 16

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

Answer 16

A: heliocobacter

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

Question 17

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

Answer 17

A: -infection, TB, fungi, heliocobacter

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

Question 18

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

Answer 18

A: chronic have scarring (fibrosis)

Question 19

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

Answer 19

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

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

Question 20

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

Answer 20

A: atrophy, metaplasia, dysplasia

Question 21

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

Answer 21

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

Question 22

Q: Describe heliobacter gastritis metaplasia.

Answer 22

A: gastric to intestinal cells

Question 23

Q: How are neoplasms classified? (2)

Answer 23

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

Question 24

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

Answer 24

A: malignant tumour of lymphoid tissue

associated with helicobacter gastritis

HELICOBACTER CAN CAUSE ADENOCARCINOMAS and LYMPHOMAS

Question 25

Q: What is the main staging system?

Answer 25

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

Question 26

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

Answer 26

A: coronary arteries (risk of myocardial infarction) carotid arteries (risk of stroke) aorta and / or iliac arteries

Question 27

Q: What is an atheroma? caused by?

Answer 27

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

Question 28

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

Answer 28

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

Question 29

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

Answer 29

A: chronic cardiac failure and sudden death (within 24hrs) heart has white patched

Question 30

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

Answer 30

A: -stable angina - dementia - chronic lower limb ischaemia

Question 31

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

Answer 31

A: -unstable angina - myocardial infarction - cerebral infarction - acute lower limb ischaemia

Question 32

Q: Compare infarction and ischaemia.

Answer 32

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

Question 33

Q: What details does a death certificate include?

Answer 33

A: 1a immediate cause of death 1b predisposing factor 1c predisposing factor 2 other factors contributing to but not directly leading to death

Question 34

Q: What's an aneurysm?

Answer 34

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