Inflammation, Autoimmunity etc...

Question 1

Name 5 situations where acute inflammation can occur.

Answer 1

Chemical damage, Microorgansims (bacteria), trauma, ischaemic necrosis, radiation damage.

Question 2

What are the main steps in the acute inflammatory response?

Answer 2

• Exudate produced, derived from blood components from adjacent capillaries.
• destroys/neutralises damaging agent.
• liquefies and removes dead tissue.
• prepares damaged area for healing.

Question 3

What are the functions of the exudate?

Answer 3

• Fluid - dilutes toxins and carries nutrients, mediators and antibodies.
• fibrin is released, function speculative.
• neutrophils actively phagocytic of living tissue but also necrotic debris.

Question 4

What are the consequences of acute inflammation?

Answer 4

Heat, pain, redness, swelling and loss of funtion.

Question 5

What are the components of the exudate?

Answer 5

Fluid, fibrin, neutrophils and a few macrophages and lymphocytes.

Question 6

Malaise, fever, pain and rapid pulse is due to what?

Answer 6

Exudate acting on the hypothalamus.

Question 7

Malaise, fever, pain and rapid pulse is due to what?

Answer 7

Exudate acting on the hypothalamus.

Question 8

Name and describe the two phases of resolution.

Answer 8

Inflammatory phase - fluid, proteins and neutrophils move into area of damage = exudation.

Proliferation phase - local cells re-grow, allow tissue function to return to normal.

Question 9

Describe fibrous repair.

Answer 9

Same inflammatory stage as resolution. Proliferation phase refers to formation of new capillary vessels, budding from nearby vessels and support cells - grow into damaged area. Fibroblasts proliferate and collaged laid down - forms scar tissue. Restoration of normal structure and function does not occur.

Question 10

Describe fibrous repair.

Answer 10

Same inflammatory stage as resolution. Proliferation phase refers to formation of new capillary vessels, budding from nearby vessels and support cells - grow into damaged area. Fibroblasts proliferate and collaged laid down - forms scar tissue. Restoration of normal structure and function does not occur.

Question 11

What can not occur in chronic information?

Answer 11

Complete healing.

Question 12

Tissue is infiltrated by specific immune effector cells, main one being what?

Answer 12

Macrophages.

Question 13

Always heals how?

Answer 13

Scarring.

Question 14

What are ineffective in granulomatous inflammation?

Answer 14

Neutrophils.

Question 15

How is a granuloma formed?

Answer 15

Macrophages aggregate around the damaging agent and associated with a surrounding lymphocyte cuff and fibroblasts form a granuloma.

Question 16

What do macrophages secrete?

Answer 16

Cytokines, mediators of inflammation, growth factor and activated gamma interferon.

Question 17

What do macrophages secrete?

Answer 17

Cytokines, mediators of inflammation, growth factor and activated gamma interferon.

Question 18

The exudate can cause symptoms such as what?

Answer 18

Meningitis, pericarditis, diphtheria.

Question 19

Name 5 reasons why inadequate healing may take place.

Answer 19

Denervation of the area, foreign/unknown necrotic material in the area, ischaemic of the region, diabetes, previous irradiation, steroid therapy, continuing infction.

Question 20

Brain necrosis - how is brain parenchyma different?

Answer 20

Does not contain fibroblasts, cannot make collagen.

Question 21

What does necrosis undergo?

Answer 21

Liquefaction - macrophages turn it in to a liquid and phagocytose the debris.

Question 22

Dead area is walled off by what?

Answer 22

Astrocytes.

Question 23

Bone - defect filled with what?

Answer 23

Blood clot.

Question 24

Like exudate, haematoma undergoes what?

Answer 24

Organisation - after the debris is phagocytosed.

Question 25

Defect subsequently filled by what?

Answer 25

Vascular then fibro-vascular granulation tissue.

Question 26

Defect subsequently filled by what?

Answer 26

Vascular then fibro-vascular granulation tissue.

Question 27

Autoimmunity - Describe Graves’ disease.

Answer 27

Beta cells produce antibodies that specifically bind to the TSH receptor expressed by thyroid follicular cells and stimulate thyroid hormone production. There is negative feedback but due to the antibodies it has not much effect therefore hyperthyroidism.

Question 28

What happens in graves’ opthalmopathy

Answer 28

Inflammatory damage of extra-ocular tissue with production of mucopolysaccharides and associated oedema behind eyes causing eyes to bulge.

Question 29

What is pre-tibial myxoedema?

Answer 29

Similiar to G.O, deposition of muco-polysaccharides in subcutaneous tissue causes swelling on front of skin.

Question 30

What is Atrophic thyroiditis?

Answer 30

When antibodies block rather than stimulate TSH receptors - leads to hypothyroidism. Ref. Hashimoto’s.

Question 31

Pernicious anaemia is caused how?

Answer 31

Autoimmune destruction of gastric parietal cells and production of autoantibodies to IF. Causes reduced B12 absorption from the gut and subsequently pernicious anaemia.

Question 32

Describe myasthenia gravis.

Answer 32

Autoantibodies specific for ACh receptors expressed on muscle cells at neuromuscular junction. Block binding site and induce internalisation and degradation of receptors.
Results in extreme weakness due to lack of nerve stimulation.

Question 33

Briefly outline what autoimmune haemolytic anaemia and Pempigus is.

Answer 33

A.H.A, production of autoantibodies specific for erythrocyte surface autoantigens inducing complement activation and destruction by phagocytes.
Pempigus, autoantibodies bind to intercellular substance of skin epidermis, induces blistering inflammation reaction.

Question 34

Briefly outline what autoimmune haemolytic anaemia and Pempigus is.

Answer 34

A.H.A, production of autoantibodies specific for erythrocyte surface autoantigens inducing complement activation and destruction by phagocytes.
Pempigus, autoantibodies bind to intercellular substance of skin epidermis, induces blistering inflammation reaction.

Question 35

Name 3 and describe one other autoimmune disease.

Answer 35

Good pasture’s disease - kidney and possibly lung damage. Systemic lupus erythematosus (SLE) - causes tissue damage. Rheumatoid Arthritis - rheumatoid factors form immune complexes - cause damage in joints.

Question 36

Name 3 and describe one other autoimmune disease.

Answer 36

Good pasture’s disease - kidney and possibly lung damage. Systemic lupus erythematosus (SLE) - causes tissue damage. Rheumatoid Arthritis - rheumatoid factors form immune complexes - cause damage in joints.

Question 37

Immunodeficiencies - what is the difference between primary and secondary immunodeficiency?

Answer 37

Primary - usually due to inherited mutations - most autosomal recessive.
Secondary - acquired as a consequence of environmental insults.

Question 38

What are bacterial, viral and fungal infections caused by?

Answer 38

Bacterial infections caused by deficiency antibodies, complement/phagocytes.
T-cell defects cause viral and fungal infections.

Question 39

Di George Syndrome is a t-cell deficiency causing what?

Answer 39

Defective development of the thymus due to developmental defect in 3rd and 4th pharyngeal arches. Deficiency causes viral and fungal infections and graft vs host disease. Defective parathyroids cause hypocalcaemia.
Defective great vessels causes congenital heart disease and defective face causes dysmporphic features.

Question 40

In HIV, t-cells are infected by binding to what? What does this cause?

Answer 40

CD4 molecules. The progressive decline in CD4 cells results in worsening immune function and increased susceptibility to infection.

Question 41

What is severe combined immunodeficiency? How is it treated?

Answer 41

Inherited, stem cell defect, lack of function of T and B cells. Presents in 1st year of life, fatal if left untreated, only treatable by bone marrow transplant