Lecture 8 : inflammation

Question 1

Megakaryocytic:

Answer 1

break up to form small platelets (thrombocytes) which play a critical role in blood clotting following their activation. Also produce pro-inflammatory cytokines and chemokines

Question 2

Monocytes / Macrophages:

Answer 2

monocytes migrate to tissues and differentiate into macrophages. Their functions are principally phagocytosis, but also antigen presentation, and cytokine production

Question 3

Basophils:

Answer 3

least common WBC, releases histamines and prostaglandins to cause dilation and increased capillary permiability

Question 4

Mast Cells:

Answer 4

key role in allergy and anaphalaxis. Contains granules of heparin and histamines as well as pro-inflammatory cytokines such as TNFalpha, IL4

Question 5

Eosinophils:

Answer 5

key role in anti-parasite responses, present antigens to the adaptive immune system, generate cytokines and kill cancer cells

Question 6

Neutrophils:

Answer 6

50-60% of circulating WBCs. Rapidly leave the circulation to home on a site of injury & inflammation where they die and form puss. They phagocytose microbes, release anti-microbials and generate extracellular neutrophil traps. They also secrete cytokines that recruit macrophages

Question 7

Blood vessels: 3 types

Answer 7

continuous, fenestrated, sinusoid

Question 8

continuous blood vessels:

Answer 8

Only small molecules. eg. Muscles, gonads, fingers, CNS

Question 9

Fenestrated blood vessels:

Answer 9

60-80nm pores allow small molecules and some proteins

Question 10

sinusoid blood vessels:

Answer 10

allow blood cells to cross e.g. bone marrow, lymph nodes

Question 11

In extreme cases positive feedback of cytokines on WBCs can turn

Answer 11

a localised inflammation into a systemic ‘cytokine storm’. Often with fatal consequences
eg. anaphylaxis, septicemia, 1918 Flu

Question 12

Chronic inflammation:

Answer 12

• long duration

- lymphocytes, plasm cells and macrophages

Question 13

acute inflammation:

Answer 13

• short duration

- neutrophils

Question 14

impact of vascular changes:

Answer 14

• Increase in permeability (e.g. histamine)
• —increase fluid influx to tissue
• Swelling – oedema
• reduction in blood velocity promotes:
• –margination
• –diapedesis

Question 15

diapedesis:

Answer 15

the passage of blood cells through the intact walls of the capillary

Question 16

early responses depend on

Answer 16

site and extent of damage. some early responses inhibited by anti-histamines

Question 17

3 types of response

Answer 17

• immediate-transient response
• immediat-peristsen response
• delayed-persistent response

Question 18

delayed persistent response:

Answer 18

radiation damage to endothelial cells

Question 19

indicators of infection:

Answer 19

• C-reactive protein
• Neutrophils (bacterial), lymphocytes (viral), eosinophils (allergy, parasites)
• HPA hormones (hypothalamic pituitary, adrenal), e.g. growth hormone, ACTH (AdrenoCorticoTropic Hormone) – a consequence of biological stress that causes increased production of cortisol

Question 20

chronic inflammation e.g.

Answer 20

TB, rheumatoid arthritis, syphilis, leprosy.

May or may not have prodding acute phase

Question 21

chronic inflammation: Osteomyelitis

Answer 21

• Chronic infection of bone

- Poor vascularisation means poor recovery

Question 22

inflammation is often

Answer 22

good: indicator of active, positive responses by the body to damage and / or infection.

Question 23

inflammation may be

Answer 23

bad : : involves mediators that may run out of control

Question 24

involves cells and mediators that are

Answer 24

also involved in immune responses, blood clotting and repair.