ICS

Question 1

What cells predominate in acute inflammation?

Answer 1

Neutrophil polymorphs.

Question 2

What cells predominate in chronic inflammation?

Answer 2

Lymphocytes, plasma cells + macrophages.

Question 3

Briefly explain the process of acute inflammation.

Answer 3

• Initial reaction of tissue to injury.
• Vascular component – vasodilation.
• Exudative component (vascular leakage of protein-rich fluid).
• Neutrophil polymorph recruitment to tissue.

Question 4

What are the cardinal features of inflammation?

Answer 4

• Redness (rubor).
• Het (calor).
• Swelling (tumor).
• Pain (dolor).
• Loss of function.

Question 5

What are the potential outcomes of inflammation?

Answer 5

• Resolution.
• Suppuration = pus formaiton.
• Organisation = repair of specialised tissues by formation of fibrous scar.
• Chronic inflammation > fibrosis.

Question 6

What is a granuloma?

Answer 6

Aggregate of epithelioid histiocytes.

Question 7

What is granulation tissue?

Answer 7

New connective tissue + small blood vessels that form on surface of a wound.

Question 8

What is the different between resolution and repair in inflammation?

Answer 8

• Resolution occurs when initiating factor is removed + tissue is either undamaged or able to regenerate.
• Repair occurs when initiating factor is still present but tissue is damaged/unable to regenerate, involves replacement of damaged tissue by fibrous tissue.

Question 9

What cells are capable of regeneration?

Answer 9

• Hepatocytes.
• Pneumocytes.
• Gut + skin epithelial cells.
• All blood cells.
• Osteocytes.

Question 10

What cells are incapable of regeneration?

Answer 10

• Neurones.

- Myocardial cells.

Question 11

Define and give an example of…

i) Apoptosis.
ii) Necrosis.
iii) Atrophy.

Answer 11

i) Programmed cell death as a result of stimuli, too much = HIV, not enough = cancer.
ii) Traumatic cell death, occurs due to infarction like MI, CVA, frostbite.
iii) Decrease in the size of a tissue caused by a decrease in the number of constituent cells/decrease in their size, seen in Alzheimer’s disease.

Question 12

Define and give an example of…

i) Hypertrophy.
ii) Hyperplasia.
iii) Metaplasia.

Answer 12

i) Increase in size of a tissue caused by an increase in size of constituent cells, building muscle.
ii) Increase in size of a tissue caused by an increase in the number of constituent cells, prostatic hyperplasia.
iii) Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type, Barrett’s oesophagus.

Question 13

Define.

i) Dysplasia.
ii) Neoplasia

Answer 13

i) Morphological changes seen in cells progressing to cancer.
ii) New + abnormal growth of tissue in the body which persists despite removal of initial stimulus.

Question 14

What is a tumour? What’s the difference between benign + malignant neoplasms?

Answer 14

• Any abnormal swelling.
• Benign = localised, slow growth rate, low mitotic activity.
• Malignant = invasive, metastases, rapid growth rate.

Question 15

What are the two types of benign epithelial neoplasms?

Answer 15

• Papilloma = benign tumour of non-glandular, non-secretory epithelium.
• Adenoma = benign tumour of glandular or secretory epithelium.

Question 16

What are the two types of malignant epithelial neoplasms?

Answer 16

• Carcinoma = malignant epithelial neoplasm.

- Adenocarcinoma = carcinoma of glandular epithelium.

Question 17

How are benign connective tissue neoplasms named?

Answer 17

Suffix -oma…

• Rhabdomyoma (striated muscle)
• Leiomyoma (smooth muscle).

Question 18

How are malignant connective tissue neoplasms named?

Answer 18

Suffix -sarcoma…

• Liposarcoma = adipose tissue.
• Angiosarcoma = blood vessels.

Question 19

What is carcinogenesis?

Answer 19

• Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations.

Question 20

What type of cancers are caused by…

i) Polycyclic aromatic hydrocarbons (smoking, mineral oils).
ii) Aromatic amines (rubber/dye workers)
iii) Nitrosamines.
iv) Alkylating agents.

Answer 20

i) Lung, skin.
ii) Bladder.
iii) Gut.
iv) Leukaemia.

Question 21

How can tumours spread?

Answer 21

• Invades basement membrane using collagenases
• Tumour motility.
• Enters lymph/blood vessels.
• Evades host immune defence.
• Triggers angiogenesis to nurture growth at new site.

Question 22

What is the likely origin of…

i) Lung metastases?
ii) Liver metastases?
iii) Bone metastases?

Answer 22

i) Sarcomas, many common (breast).
ii) Colorectal, stomach, pancreas, carcinoid of intestine.
iii) Prostate, breast, thyroid, lung + kidney.

Question 23

What is innate immunity?

Answer 23

• Non-specific, instinctive, present from birth + first line of defence.

Question 24

Name some components of the innate immune system.

Answer 24

Physical + chemical barriers…
- Mucous in resp tract, skin as physical barrier, low vaginal pH, acidic gut.
Phagocytic cells like neutrophils + macrophages.
Serum proteins like complement, acute phase proteins.

Question 25

What ways can complement activation occur?

Answer 25

``` Classical pathway... - Antibody-antigen immune complexes. Alternative pathway... - Foreign surfaces-antigens. Lectin pathway... - Mannose-binding lectin, mannose residues on pathogen surface. ```

Question 26

What is the complement pathway?

Answer 26

- Lyse microbes directly (formation of membrane attack complex). - Increase chemotaxis, cell recruitment (C3a + C5a). - Opsonisation (increasing phagocytosis, C3b).

Question 27

What is adaptive immunity?

Answer 27

- Specific, requires lymphocytes, memory + quicker response.

Question 28

What is the major histocompatibility complex? What are the two classes?

Answer 28

Proteins that mark a cell as SELF. Class I = all nucleated cells (not RBCs) - E.g. virus infected or cancer cell. Class II = certain immune cells, antigen-presenting. - E.g. macrophages, B cells, dendritic cells.

Question 29

What are pattern recognition receptors?

Answer 29

- Secreted + circulating like lectins and collectins. | - Cell associated like toll/nod-like receptors.

Question 30

What are the things are recognised in relation to pattern recognition receptors?

Answer 30

- Pathogen associated molecular patterns (PAMPs) like lipopolysaccharides. - Damage associated molecular patterns (DAMPs).

Question 31

Where are T lymphocytes produced + matured? How do T cells recognise antigens?

Answer 31

- Produced in bone marrow, mature in thymus. | - Must be displayed by an antigen presenting cell bound to MHC1/2.

Question 32

What are the two types of T cells?

Answer 32

Cytotoxic T cells (CD8)... - Destroy infected body cells (apoptosis) by binding to antigens. - Binds to MHCI. T helper cells (CD4)... - Binds to MHCII. - Th1 secretes cytokines. - Th2 activates eosinophils, basophils, induce B cells to make antibodies by releasing cytokines to induce B-cell proliferation.

Question 33

Where are B lymphocytes produced + matured? What do they do? How are they activated?

Answer 33

- Produced + mature in bone marrow. - Recognise soluble, free, native, polypeptide antigens. - Travel to lymph nodes where they proliferate + differentiate into plasma cells (secrete antibodies) + memory B cells (immunity).

Question 34

What are the functions of antibodies?

Answer 34

- Neutralise toxins. - Opsonisation. - Activate classical complement system.

Question 35

What are the different types of antibodies?

Answer 35

- IgM = made first. - IgG = most common, crosses placenta (passive immunity). - IgA = secreted from mucous membranes (breast milk). - IgD = B cella ctivation. - IgE = histamine reactions + allergies.

Question 36

What is the Fab and Fc region of antibodies?

Answer 36

- Fab region is part that binds to epitope of an antigen. | - Fc region is part that binds to B cells.

Question 37

What does specific binding of the Fab region lead to?

Answer 37

- Neutralise toxins (IgG, A). - Immobilise motile microbes (IgM). - Prevent binding to + infection of host cells.

Question 38

What are the enhance innate mechanisms with the Fc region?

Answer 38

- Activate complement (IgG, M). Bind Fc receptors... - Phagocytes (IgG, A) enhances phagocytosis. - Mast cells (IgE) release inflammatory mediators. - Natural killer cells (IgG) enhanced killing of infected cells.

Question 39

What is hypersensitivity?

Answer 39

- The immune system responds inappropriately to a normal harmless antigen.

Question 40

What is a type 1 hypersensitivity reaction

Answer 40

- IgE mediated, allergic + acute. - IgE binds to mast cells causing histamine release. - Anaphylaxis, hayfever.

Question 41

What is a type 2 hypersensitivity reaction

Answer 41

- IgG bound to cell surface antigens/IgM | - Transfusion reactions, autoimmune disease, goodpastures.

Question 42

What is a type 3 hypersensitivity reaction

Answer 42

Immune complexes, activation of complement/IgG. | - SLE.

Question 43

What is a type 4 hypersensitivity reaction

Answer 43

T-cell mediated delayed type hypersensitivity. | - TB, contact dermatitis.

Question 44

Briefly describe immunity.

Answer 44

First exposure... - IgM made first, rapidly increases. - IgG begins to be made, rapidly increase. - IgM decreases first, IgG decreases after. Second exposure... - IgG RAPIDLY produced in vast quantities. - Small rise in IgM. - Symptoms not experienced second exposure.

Question 45

What is the aim of vaccinations?

Answer 45

- Achieve long-term protection, stimulate both B+T cells, induce memory B+T cells + stimulate protective high affinity IgG production.