Pathology

Question 1

Describe the 6 types of necrosis?

Answer 1

Coagulative – proteins coagulate, preservation of cell outline e.g. MI
Colliquative – necrotic material becomes softened and liquefied (PUS), no cell structure remains e.g. Brain necrosis
Caseous – cheese like – e.g. TB
Gangrenous – cell death by necrosis then infection on top of it – anaerobic bacteria may grow
Fibrinoid – fibre deposition eg damage to blood vessel in malignant hypertension
Fat necrosis – acute pancreatitis

Question 2

What enzyme stimulates caspases and indices apoptosis if DNA cannot be repaired?

Answer 2

p53

Question 3

Describe telomeres and cancers affect on them?

Answer 3

chromosomes are capped to prevent degradation and fusion
with every division the number of repeats gets smaller
telomerase adds on TTAGGG after its lost preventing cells from dying

cancer reactivates telomerase and can become immortal

Question 4

Describe acute inflammation?

Answer 4

Initial, often transient series of tissue reactions to injury
Vascular phase - vasodilatation and increased permeability of blood vessels
Exudative and cellular phase - fluid and cells escape from permeable venules through margination
Neutrophil accumulation in extracellular space

Question 5

Describe chronic inflammation?

Answer 5

Subsequent and often prolonged tissue reactions following initial response
Recurrence of acute inflammation may lead to chronic
More likely if: scarring or pus or if the injury is autoimmune

Question 6

What are inflamed organ surfaces usually covered in?

Answer 6

Fibrin (fibrogen changes to fibrin on contact with the ECM)

Question 7

How do neutrophils reach the inflammation?

Answer 7

Margination – loss of intravascular fluid and increased plasma viscosity allows neutrophils into plasma (only occurs in venules)
Adhesion
- Surface adhesion molecule expression increased by
Complement C5a
Leukotriene B2
TNF
- Endothelial cell expression of adhesion molecules increased by
IL1
Endotoxins
TNF
Transendothelial migration

Question 8

What is chemotaxis?

Answer 8

cells follow eachother along a chemical gradient

Question 9

Briefly describe the actions of the 5 chemical mediators/

Answer 9

Histamine – vascular dilation
Released by mast cells, eosinophils, basophils, platelets neutrophils
Serotonin – increased vascular permeability
5HT present in high concentration in platelets
Chemokines - Attract various leucocytes to site of inflammation
Leukotrienes – type 1 hypersensitivity
Prostaglandins – increase vascular permeability, stimulate platelet aggregation

Question 10

What is suppuration?

Answer 10

Formation of pus from neutrophils, bacteria, cellular debris

Question 11

What is resolution?

Answer 11

Complete restoration of tissues to normal after episode of acute inflammation

Question 12

What are the cells of chronic inflammation?

Answer 12

Plasma cells - formed from B lymphocytes
T Lymphocytes - produce cytokines
Macrophages

Question 13

What is a granuloma and what is granulation tissue?

Answer 13

Granuloma: collection of macrophages

Granulation tissue: undergoes organisation to form fibrous scar

Question 14

What is irreversible damage?

Answer 14

Severe damage to cell membranes and mitochondria
Leakage of enzymes
Nuclear changes – ATP changes, cell membrane damage

Question 15

What is reversible damage?

Answer 15

Reduced aerobic respiration/increased anaerobic
Membrane pumps fail
Cell swelling
Accumulation of lipids

Question 16

What is differentiation?

Answer 16

development of a specialised function

Question 17

What is hyperplasia?

Answer 17

Increase in cell number

- at risk site for cancer development

Question 18

What hypertrophy?

Answer 18

Increase in cell size

- e.g. cardiac myocytes

Question 19

What is atrophy?

Answer 19

reduction in cell size and number

Question 20

What is metaplasia?

Answer 20

change of cell in some form due to a change in stimulus

- reversible

Question 21

What is hypoplasia?

Answer 21

reduced size of an organ that never fully developed to normal size

Question 22

What is dysplasia?

Answer 22

disordered growth
Low grade = normal
High grade = closer to being cancer

Question 23

What is neoplasia?

Answer 23

new growth not in response to a stimulus
can be benign, malignant or premalignant
epithelial cells are most common type of malignancy

Question 24

Describe benign neoplasia?

Answer 24

o	No necrosis 
o	N:C (nucleus Cytoplasm) ratio normal 
o	Minimal pleomorphism (change in size/shape)
o	Diploid 
Can be called:
Adenoma 
Papilloma

Question 25

Describe malignant neoplasia?

Answer 25

o	Necrosis common 
o	N:C ratio increased 
o	Pleomorphic 
o	Aneuploid 
Can be called:
Carcinoma – cancer of epithelial cell
Carcinoma in situ – not invading other tissues, confined to site of origin
Sarcoma – cancer of mesenchymal cell

Question 26

What is angiogenesis?

Answer 26

Formation of new, abnormal blood vessels

Successfully growing tumours will develop ability to create own blood supply

Question 27

What is the double hit hypothesis?

Answer 27

One working gene is enough.
One faulty gene puts person at increased risk.
Two faulty mutated genes will result in a functional problem.

Question 28

What are metastasis?

Answer 28

Formation of tumour implants that are discontinuous with the primary lesion
- Routes
Lymphatic = Carcinoma
Haematogenous = Sarcoma

Question 29

Name the 3 steps of cancer progression

Answer 29

1. Initiation - 1st mutation (e.g. oncogene, tumour suppressor, DNA repair, evasion of apoptosis)
2. Promotion –further accumulation of mutations
3. Persistence –unregulated abnormal growth, can become malignant.

Question 30

What are oncogenes?

Answer 30

turn up genes that promote cancer growth

Question 31

What are tumor suppressors?

Answer 31

turn off genes that slow growth

• Inhibit cell proliferation
• Stimulate cell death
• Recessive

Question 32

Name some commonly found bengin and malignant cancers?

Answer 32

Epithelium – carcinomas
Glandular – adenoma v adenocarcinoma (malignant)
Squamous – papilloma v Squamous cell carcinoma