Immunology, Inflammation And Repair

Front 1

5 signs of inflammation

Back 1

heat,
redness,
swelling,
pain,
injured or impaired function.

Front 2

what is inflammation

Back 2

the reaction of vascularised living tissue to local injury

Front 3

When an organ is inflamed, a name is given to it

Back 3

that organ, with the suffix “itis” on the end

For example, inflammation of the liver is termed hepatitis, inflammation of the skin is termed dermatitis and inflammation of the intestine is called enteritis.

Front 4

causes of cell damage leading to inflammation (4)

Back 4

chemical (drugs, toxins)

physical (Trauma, pressure, heat, cold, radiant energy / UV and sunlight)

infectious (bacteria, viruses, fungi, protozoa, parasites)

immune response (hypersensitivity and autoimmunity)

Front 5

foreign agents leading to inflammation

Back 5

Infectious agents (Bacteria, viruses, fungi, protozoa, parasites), or

foreign bodies (pollens, splinters, inhaled food etc)

Front 6

T/F

Inflammation only occurs in living tissues

Back 6

T

Inflammation cannot occur in a dead organism. The inflammatory process depends wholly on viable tissue.

Front 7

T/F

Inflammation can be harmful.

Back 7

T

Inflammation can be harmful.
In many situations, the host may suffer more tissue damage as a result of the inflammatory reaction than would have been caused by the initiating stimulus had there been no inflammatory response.

It is for this reason that anti-inflammatory drugs are often used to limit the effects of inflammation.

Front 8

white blood cells and serum proteins, platelets, coagulation factors, fibrinolytic enzymes and antibody are delivered to where they are needed by

Back 8

the circulation, in the blood

Front 9

T/F

Much of the inflammatory response is surface orientated.

Back 9

T

Much of the inflammatory response is surface orientated.
Since leucocytes can neither see nor hear they depend on their cell membrane to act as their eyes and ears. The stimulus involves surface membrane receptor activation that then activates intracellular events that are specific for cellular function.

Front 10

antigen

Back 10

antigens are biochemical/chemical groups capable of being detected and responded to by the immune system

Front 11

Innate mechanisms include

Back 11

physical and physiological barriers to agents of disease (commonly operate on surfaces normally exposed to foreign antigens eg muco-ciliary escalator in the lungs, keratin layer of skin), host chemicals (eg lysozyme) and host cells (eg phagocytes such as neutrophils).

Front 12

Adaptive immunity involves

Back 12

a recognition and response to specific foreign antigens

Adaptive mechanisms also involve host chemicals (eg cytokines) and host cells (eg lymphocytes)

response is adapted to a specific foreign antigen, it is usually more effective in removing the agent of disease.

acts by

- enhancing the action of innate immunity (eg mobilizing increased numbers of neutrophils, enhancing phagocytic capacity)

- specific mechanisms eg (antibody and cell mediated destruction or neutralization of foreign antigens)

Front 13

Repair is usually through a combination of regeneration of constituent cells and replacement by fibrovascular tissue that matures into scar tissue. The relative proportions of regeneration and replacement depends on

Back 13

the tissue affected (eg cardiac muscle cells do not regenerate whereas hepatocytes have a high capacity to regenerate) and the severity of the damage (eg if the tissue framework is severly disrupted then scarring is highly likely).

Front 14

give an example of the “imperfect equilibrium" arms race between pathogen and host adaptations

Back 14

Intracellular survival and replication within phagocytes by certain microbes

Mycobacterium bovis, chlamydial infection in the koala,

Front 15

draw a diagram / flow chart of the possible outcomes of an inflammatory lesion

Back 15

Front 16

colonisation

Back 16

an outcome of infection whereby a microbe exists and replicates on a host surface without causing disease (Colonisation may progress to invasion and produce disease, which may be clinical or rubclinical, local or systemic depending on HPEI) primarily applied to microbes in skin and mucosal surfaces.

Front 17

commensals

Back 17

microbes that establish an inoffensive relationship with the host through colonisation, though altered HPEI can cause them to become pathogenic.

commensualism can be considered equivalent to colonisation, but is usually used to describe microbial flora of skin and mucous membranes which are usually found in that host species

Front 18

compromise

Back 18

an altered state where the host is susceptible to disease agents

Front 19

disease

Back 19

disturbance of structure or function in the hosts tissues, caused by an agent of disease or the hosts response. may manifest clinically or may be subclinical (detected only by specialist investigation)

Front 20

environment

Back 20

external conditions that surround act upon and influence the host and pathogen.

physical habitat, climate, social structure, flora and fauna, conspecfics, commensuals and environmental microbes separate to the pathogen

Front 21

exposure

Back 21

potential for contact between host and pathogen, at the point of contact, exposure becomes infection

Front 22

host

Back 22

the entity in which the potential for disease is being studied

may be an individual or a population

Front 23

host immunity / defence

Back 23

the attempt by the host to resist and remove an agent of disease, innate and adaptive immunity, surface defence mechanisms, protective behaviours, inflammation and repair

Front 24

infection

Back 24

any direct contact between the host and the pathogen, with or without the manifestation of disease

Front 25

infectious agents of disease

Back 25

replicating agents of disease such as bacteria, fungi, viruses, prions, protozoans, metazoans, and rarely algae

Front 26

invasiveness

Back 26

the capacity of microbes and other agents of disease to penetrate cells or tissues, often includes their capacity to multiple within tissues.

Front 27

latency

Back 27

where an organism persists in a dormant state after infection of the host. subclinical or clinical disease is induced before latency is established, and an organism might emerge from latency to induce further disease. during latency a disease is not progressive.

Front 28

parasite

Back 28

an organism that lives on or in a host, from which it obtains nourishment, during all or part of its existence. includes microbes such as bacteria, protozoa algae virsuses fungi metazoans

Front 29

pathogenesis

Back 29

the origin and course of development of a disease

Front 30

pathogen

Back 30

disease causing agent

Front 31

pathogenicity

Back 31

capacity of an agent of disease, to produce diseaase, agents of low pathogenicity might cause disease in a compromised animal, but rarely in a normal animal

Front 32

saprophyte

Back 32

an environmental microbe that lives on dead or decaying matter

Front 33

virulent microbes

Back 33

organisms that have high likelihood of causing clinical disease. Virulence usually refers to the relative pathogenicity of strains of microbes within a species. Some strains may be highly virulent while others may have low virulence or may even be avirulent. This tends to focus on pathogen factors of the HPEI.

Front 34

The cardinal local signs of inflammation are redness, swelling, pain, heat and loss of function. What causes these?

Back 34

The local heat and redness are the result of dilation of the microcirculation in the local environment. The swelling is largely due to the escape of fluid containing plasma proteins and other solutes from the blood to the perivascular tissues. Leucocytes also escape and the high protein content of the fluid with the presence of leucocytes is known as exudation. The origin of the pain is multifactorial but can be attributed to irritation of local nerves by biochemical mediators. Loss of function occurs due to damage to physiology and anatomy of local structures.