Pathology

Question 1

What does VINDICATE stand for?

Answer 1

Vascular
Infectious/Inflammatory
Neoplastic
Drugs/toxins
Intervention/iatrogenic
Congenital/developmental
Autoimmune
Trauma
Endocrine/metabolic

Question 2

What are the vascular changes in acute inflammation?

What are they mediated by?

Answer 2

Vasodilation

Mediated by NO and histamine

Question 3

What are the cellular changes in acute inflammation?

Answer 3

Stasis
White Cell Margination
Rolling
Adhesions (integrin/selectins, VCAM/ICAM)
MIgration

Question 4

What causes leaky vessels?

Answer 4

Endothelial contraction
Direct injury
White cells
Transcytosis
New vessel formation

Question 5

What are the 3 stages of phagocytosis?

Answer 5

Recognition and attachment
Engulfment
Killing and degradation

Question 6

How do phagocytes recognise pathogens?

Answer 6

Mannose receptors

Opsonins

Question 7

What are the clinical features of acute inflammation?

Answer 7

Redness (rubor)
Heat (calor)
Swelling (tumor)
Pain (dolor)
Loss of function

Question 8

What is the main cell of acute inflammation?

Answer 8

The neutrophil

Question 9

What are the 4 possibilities after acute inflammation?

Answer 9

Resolution (good as new)
Suppuration (pus - neutrophils)
Repair, organisation and fibrosis (scarring)
Chronic inflammation

Question 10

What does the result of acute inflammation depend on?

Answer 10

Site of injury
Type of injury
Duration of injury

Question 11

What is the main cell of chronic inflammation?

Answer 11

Macrophage

Question 12

What is a granuloma?

Answer 12

An aggregate of epitheliod histiocytes (a group of inflammatory cells)

Question 13

What is hyperplasia?

Answer 13

Increase in cell number

Question 14

What is hypertrophy?

Answer 14

Increase in cell size

Question 15

What is atrophy?

Answer 15

Reduction in cell size

Question 16

What is metaplasia?

Answer 16

Reversible change from one mature cell type to another mature cell type

Question 17

What are the types of necrosis?

Answer 17

Coagulative necrosis (preservation of cell outline)
Liquefactive necrosis (liquid viscous mass - no cell structure)
Caseous nerosis (granulomatous inflammation with central necrosis)

Question 18

What is apoptosis?

Answer 18

Programmed cell death in response to specific signals

Question 19

How does extrinsic apoptosis occur?

Answer 19

Death receptor initiated pathway (TNF, Fas)

Question 20

How does intrinsic apoptosis occur?

Answer 20

Increased permeability of mitochondria allows release of proteins that stimulate caspases

Question 21

What are chromosomes capped by?

Answer 21

TTAGGG repeats

Question 22

Why do cells naturally die?

Answer 22

Telomeres become too short and apoptosis is activated

Question 23

What is neoplasia?

Answer 23

New growth, not in response to a stimulus

Question 24

What is a malignant tumour?

Answer 24

A tumour with metastatic potenital

Question 25

What is dysplasia?

Answer 25

Disordered growth leading to abnormal cells

Question 26

What is carcinoma-in-situ?

Answer 26

The last stage of dysplasia before a tumour becomes malignant Dysplasia affecting the whole of the epithelial (but not crossing the basement membrane)

Question 27

What is the double hit hypothesis?

Answer 27

People who have already inherited a faulty gene are a higher risk of developing a tumour etc, because they only need one mutation in the normal gene to have an effect

Question 28

What are the 3 types of growth receptors?

Answer 28

Receptors with intrinsic tyrosine kinase activity 7 transmembrane G protein-coupled receptors Receptors without intrinsic tyrosine kinase activtiy

Question 29

What impacts can cancer have?

Answer 29

``` Mass effect Loss of function Lack of energy, weight loss (cachexia) Infiltration (invasion of other structures) Paraneoplastic syndromes Immunosuppression Metastases ```