Immunology in context Flashcards

(39 cards)

1
Q

Inflammation

A

Reaction of vascularised living tissue to local injury

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2
Q

Repair

A

Replacement of injured tissue by: a) regeneration b) fibroblastic or glial scar tissue

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3
Q

Acute inflammation features

A

Rapid onset, short duration, stereotyped response, rapid resolution.

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4
Q

Vascular changed in acute inflammation

A

Initial vasoconstriction, then vasodilation and increase in blood flow. Increased permeability causing leaking of fluid to extracellular space.

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5
Q

Oedema

A

Collection of extracellular fluid within tissues.

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6
Q

Acute Serous inflammation

A

Acute inflammation when fluid accumulation is a dominant feature of inflammation.

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7
Q

Exudate in acute inflammation

A

Extravascular fluid with high protein concentration and cellular debris.

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8
Q

Pus

A

A thick exudate rich in leukocytes (neutrophils) and cell debris.

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9
Q

Margination and mechanisms behind it.

A

Margination: rolling over and slowing down of neutrophils and molecules due to adherens to epithelial cell membrane

Mechanisms: Weide-palade cells secrete P and E selectin which migrate to the endothelium where they attract neutrophils and cause them to slow down.

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10
Q

Chemotaxis what it is, 1 example of chemokine and 3 examples of chemokine inducing agents (that cause release of chemokine)

A

The unidirectional migration of cells (neutrophils) towards a chemokine secreted by the inflamed cell.

IL-8 example of chemokine

3 examples:

  1. Bacterial products
  2. Complement system components like c5a
  3. products of lipoxygenase pathway of arachidonic acid metabolism (leukteiene B4)
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11
Q

Diapedesis and Extravasation

A

interaction between integrin molecules and endotheilial adhesion molecules such as ICAM-1. cause movement of cells across endothelium (diapedisis) and into tissues following chemokine gradient (exravasation)

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12
Q

Characteristics of chronic inflammation

A

Associated with presence of mononuclear cells (lymphocytes, macrophages, plasma cells)

proliferation of blood vessels and connective tissue

not always the same

long term.

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13
Q

Causes of a chronic inflammation that are not following an acute inflammation

A

Persistent infection by intracellular organisms

Exposure to non-degradable substance (e.g. coal)

Autoimmune disease.

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14
Q

Chronic granulomatous inflammation and example.

A

primary immunideficiency disease in which macrophages collect but are unable to kill off the pathogen. Creates a big lump of cells

Example: pulmunary tubercoulosis

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15
Q

Hypersensitivity, what it is and what molecules mediate it (3).

A

Immune response due to an allergen. Mediated by IgE, mast cells and Th2 response.

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16
Q

Immediate hypersensitivity response

A

mast cell degranulation and histamine release, causing wheal and flare (raised lesions and surrounding redness)

17
Q

Autoimmunity

A

Loss of immunological tolerance to self

18
Q

Autoimmune disease and classfications

A

Autoimmunity associated with pathology. Can be organ specific (diabetes, grave’s disease) or non organ specifc (lupus, rheumatoid arthritis).

19
Q

How to prove autoimmunity? (2 ways)

A
  1. Passive transfer of disease by immune effectors (e.g. IGg antibody from mother to child) 2. Patient gets better after immunity supression.
20
Q

Graves’ thyroiditis Disease

A

Inflammation behind the eyes. Autoimmune disorder where anti-thyroid autoantibodies bind to thyroid stimulating hormone receptor (thyroid) overactivating them so overproduction of thyroxine.

21
Q

Myasthenia Gravis

A

Antibody binds to acetylcholine receptors at neuromuscular junction and inactivates it, causing muscular weakness and fatigue.

22
Q

Immunological role of T cells in Type I diabetes

A

CD8 t cells mediated killing of T cells

CD4 mediated support of CD8 t cells

Failure of Treg to suppress

23
Q

Primary immunodeficiency and example.

A

Rare inherited defect in immunological system. Di Deorge Syndrome, SCID

24
Q

Secondary immunodeficiency and example.

A

Common acquired defect in immunological system.

25
Di George syndrome
No thymus so no T cells produced (Primary)
26
SCID (Severe Combined Immune Deficiency)
Pathways producing pre B-cell and T-cell disrupted. (primary) No b or t cells.
27
Chronic Granulomatous Disease
Inability of macrophages to form reactive oxygen compound to kill ingested bacteria. (Primary)
28
Hypergammaglobinemia
Inability to differentiate B cell into plasma cell due to mutation of gene coding for CD40 which is present on plasma B cell surface.
29
Effect of HIV virus
Infects CD4 T-cells throught CD4 receptors which stop working.
30
Treatment for AIDS
HAART: Highly Active Antiretroviral Therapy. Stabilises loss of CD4 and controls HIV infections.
31
Iatrogenic immune deficiency
When immune based therapies cause secondary immune abnormalities.
32
Immunological basis of cancer
Immune system naturally surveilles the body for cancerous cells. Overactivation of immune control mechanisms (Treg) can cause this surveillance to be stopped.
33
PD1 and PDL1 treatment for cancer functioning
Interaction between controlling molecule (Treg) and cells inhibited with PDL1 and PD1 antibodies, letting more immunosurveillance occur.
34
3 steps of neutrophil mobilization in inflamation
1. Margination 2. Chemotaxis 3. Extravasion
35
Examples of acute membranous/ suppurative and fibrinous inflammation
Membranous: pseudomebranous colitis (caused by antibiotics that kill gut flora in colon) Suppurative: apendicitis Fibrinous: penumonia
36
Outcomes of acute and chronic inflammation
37
Role of Th2 in allergic response (from T cell to mast cell degranulation)
38
Common allergic diseases and therapies. Rare therapies
39
What is the concept of immunological self tolerance?
Controlled faileure to respond to self despide being able to do so.