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Flashcards in MOD Deck (52)
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1

What is healing by primary and secondary intention?

Primary - Minimal scarring, epidermis regenerates

Secondary - Scab form, more scarring, 

2

What are the 5 signs of acute inflammation?

Redness, swelling, heat, pain, loss of function

3

What is reperfusion injury?

Ischaemia followed by return of blood results in inflammation and oxidative damage.

4

What structural changes occur during reversible and irreversible hypoxia?

Reversible - Chromatin clumping, swelling, detachment of ribosomes from RER, cytoplasmic blebs

Irreversible - lysosome lysis, ER lysis, membrane defects, shrinkage chromatin, fragmentation chromatin, dissolution chromatin,

5

What are the 4 types of necrosis

Coagulative - Protein denaturation dominates. Leaves ghost outlines.

Liquifactive - Enzyme degradation dominates. Infection

Fat necrosis

Caseous necrosis - TB

6

Difference between dystrophic and metastatic calcification?

Both deposition of calcium in tissues

Metastatic - due to elevated serum calcium

Dystrophic - due to abnormalities of tissue

7

What is hereditary angio-edema? How is it treated?

Disorder of C1 inhibitor, results in excess bradykinin release and edema.

Treat with C1 inhibitor infusion.

8

List 5 cells involved in chronic inflammation

Macrophages, lymphocytes, plasma cells, eosinophils, giant cells

9

Main cell involved in acute inflammation?

Neutrophils

10

Describe the process of fibrous repair

  1. Clot formed and Inflammatory cells invade.
  2. Clot replaced with granulation tissue. Fibroblasts migrate and produce ECM
  3. Fibroblasts contract to reduce volume. Scar occurs.

11

What are 2 methods through which growth factors can reach a cell?

  1. Extracellular signals via hormones etc.
  2. Loss of contact between adjacent cells and basement membrane

12

What is virchow's triad?

Factors that influence thrombosis formation.

  1. Abnormalities in blood vessel wall
  2. Abnormalities of blood flow
  3. Abnormalities of blood components

13

How would you treat a DVT?

Prevention - stockings, leg compression, heparin IV.

Treated - IV heparin, warfarin.

14

What is an atheroma, arteriosclerosis and atherosclerosis?

Atheroma - Lipid accumulation in tunica intima of arteries

Arteriosclerosis - Hardening of arteries due to atheroma

Atherosclerosis - Hardening of arteries due to DM or hyeprtension

15

Describe how atheromas occur

  1. Cholosterol accumulates in endothelium due to endothelial damage e.g. smoking.
  2. Macrophages enter wall and attempt to digest cholesterol and become foam cells
  3. Foam cells die and release contents
  4. Calcium salts and fibrous tissue accumulates and forms hard plaque.
  5. Endothelium over plaque ruptures and exposes collagen, recruiting platelets and forming platelet plug.
  6. Plug causes blood clot which can break off or result in ischaemia.

16

How would you differentiate a benign from malignant neoplasm?

Benign - round outer margin

Malignant - Irregular outer margin, may show necrosis

17

What needs to occur to a cell for it to form a tumour?

Tumour suppressor genes turned off and proto-oncogenes need to be turned on

18

How would you differentiate a benign and malignant neoplasm histologically?

Bengin - well differentiated, nuclei same size.

Malignant - well to poorly differentiated, nuclei different size

19

What alterations does invasion require?

  1. No adhesion between adjacent cells – reduction in E-cadherin
  2. No adhesion to basement membrane – reduction in integrin.
  3. Degradation of the basement membrane – Expression of proteases

20

What is xeroderma pigmentosa? Pattern of inheritance?

Autosomal recessive.

Cannot DNA nucleotide excision repair. Sensitive to UV --> mutations.

21

What is ataxia telangiectasia?

Cannot repair radiation damage. Lymphoid malignances.

22

What is hereditary non polyposis colon cancer syndrome?

Mutation in DNA mismatch repair genes.

Colon carcinomas.

23

What genes are associated with:

  1. Familial Adenomatous Polyposis
  2. Breast cancer
  3. Retinoblastoma

  1. APC
  2. BRCA1/2
  3. RB

24

What is TNM staging? How is it used?

T = Size of primary tumour, T1 --> T4
N = Extent of regional node metastasis, N0 (no lymph node involvement) --> N3 (involvement of an increasing number of nodes)
M = Extent of distant metastatic spread, M0 (none) --> M1 (blood borne metastases)

25

Explain Dukes staging for colorectal carcinomas

Stage A – Invasion into but not through the bowel

Stage B – Invasion through Bowel wall

Stage C – Involvement of lymph nodes

Stage D – Distant metastases

26

What is grading of a cancer?

Level of differentiation of cancer. Less differentiated = more aggressive.

27

How does radiotherapy kill a cancer?

Triggers apoptosis by direct or ROS DNA damage that is detected by cell checkpoints.

28

How does chemotherapy kill cancers?

Alkylating drugs - Cross links DNA helix and promotes apoptosis.

Antimetabolites - Attach to DNA and prevents further replication occurring.

29

Give the tumour markers found in:

a) colon, pancreas, lung, stomach, heart

b) testicles

c) liver

a) carcinoembryonic antigen

b) HCG

c) alpha fetoprotein

30

what is metaplasia

reversible change of 1 differentiated cell to another