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Symposia > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the oral microbiome?

A

Refers to microorganisms found in the human oral cavity, commensal populations don’t cause harm but can become pathogens
In health the oral microbes are mainly gram-positive and aerobic

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2
Q

What is immunology?

A

The study of all aspects of the immune system

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3
Q

What are external barrier again infections?

A
  • Skin
  • Mucus production as a lubricant and protective layer
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4
Q

What are the different immune responses?

A
  1. Innate - detect foreign bodies based on proteins sequences
  2. Adaptive - use for specific against invading pathogens
    - this also contains the memory component of the immune response
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5
Q

What is Haematopoietic differentiation?

A

When Haematopoietic stem cells in bone marrow differentiate into myeloid or lymphoid cells (2 groups of white blood cells)

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6
Q

What is a progenitor cell?

A

Cells that originate from stem cell differentiation

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7
Q

What do Lymphoid progenitor cells make?

A

T and B lymphocytes which are responsible for the antibody cellular mediated response
- make plasma cells

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8
Q

What do Myeloid progenitor cell make?

A

Varies myeloid cell linages e.g. erythrocytes, neutrophils…

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9
Q

What is the hormonal component of the immune system?

A
  1. Immunoglobulins - produced by plasma cells in thr adaptive immune system, aid in pathogenic destruction
  2. Complement - hormonal mediator
  3. Cytokines - hormonal mediator
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10
Q

What is immunoglobulin A?

A
  • IgA
    This is a mucosa specific antibody and uniquely adapted to bind to pathogens
    Present in tears, saliva and mucus
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11
Q

How is the gingival sulcus protected by neutrophils.

A
  1. Neutrophils rolls long the surface, and in this process form bond with the epithelial surface and is slowed down due to these adhesions
  2. Neutrophil slows down and adheres to the surface due to selectin and integrins interactions
  3. Gets through endothelial layer due to adhesion molecules which pull them through (PECAM-1)
  4. Gets through basement membrane by breaking it via secreting collagenase
  5. Neutrophil travels to area of inflammation
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12
Q

What is Diapedesis?

A

The mechanism in which neutrophils pass through blood vessels

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13
Q

What is inflammation?

A

A localised physiological condition where part of the body becomes red, swollen, hot and painful due to injury or infection

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14
Q

What are the different types of inflammation?

A
  1. Localised inflammation
  2. Chronic inflammation- occurs when injury is not resolved
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15
Q

What is phagocytosis?

A

Phagocyte engulfs a microorganisms and uses lysosomes to digest the microb

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16
Q

Where are macrophages found?

A

Found in areas with high infection rates e.g. lungs, lymph nodes

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17
Q

What are cytokines?

A

Proteins secreted by cells and used for cell signalling
- when monocytes secrete them it’s called monokines
- when lymphocytes secrete them it’s called lymphokines

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18
Q

What are inflammatory mediators?

A

A molecule that acts as a messenger and acts on the blood vessels or other inflammatory cells to regulate the inflammatory response

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19
Q

What are some examples of inflammatory mediators?

A
  1. Histamine - causes vasodilatation, increasing vascular permeability
  2. Chemokines - activate leukocytes and chemotaxis
    ….
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20
Q

What are the 5 steps of inflammation?

A
  1. Recognition
  2. Recruitment of leukocytes
  3. Removal of inflammatory stimuli
  4. Regulation of response (stopping inflammation avoiding chronic inflammation)
  5. Repair
21
Q

What are the differences between chronic and acute inflammation?

A
  1. Onset - acute is much faster
  2. Cells used - acute mainly used neutrophils whereas chronic uses monocytes and lymphocytes
  3. Systemic signs - chronic has little signs whereas acute is prominent
  4. Tissue damage - chronic causes sever damage to tissue
22
Q

What are causes for inflammation?

A
  1. Tissue necrosis
  2. Infection
  3. Foreign bodies
  4. Immune reaction - can be caused by auto-immune diseases
23
Q

What are the 3 major comments to acute inflammation?

A
  1. Dilation of capillaries leading to increased blood flow
  2. Increased permeability therefore plasma and leukocytes leave blood circulation
  3. Emigration of leukocytes from circulation to site of inflammation
24
Q

What does exudation of capillaries mean?

A

This is when blood plasma and proteins leave the circulation into interstitial tissue

25
Q

What does transudate of capillaries mean?

A

This is when the interstitial tissue protein content is low and has few plasma cells

26
Q

What vascular changes happen in inflammation?

A
  1. Vasodialation - caused by the effect histamine has on smooth vascular muscle
    - this opens new capillary beds Which gives blood more directions to flow
    - this slows down the flow rate in the area leading to redness due to congestion
  2. Increased concentration of red blood cells cause a thicker blood
27
Q

How is vascular permeability changed cellularly?

A
  • The gap between Endothelial cells is increased this is called the interendothelial gap, this provides a passage for plasma and leukocytes to leaves the capillary
  • This can be achieved via inflammatory mediators e.g. histamine or mechanically e.g. endothelial injury
28
Q

How does leukocytes enter the tissue?

A

This is a multi-step process:
1. Leukocytes rolls on the surface of the tissue
2. Leukocytes adhere to tissue due to adhesion molecules
3. Transmigration - leukocyte is pulling into the tissue
4. Chemotaxis - leukocytes is taken to site of inflammation

29
Q

How does the Leukocyte adhere to tissue surface?

A

Leukocyte needs to be stopped against flow:
1. Selectin - 3 types
L - on leukocyte
E - on endothelium
P - on endothelium
2. Integrins - on the surface of leukocytes

30
Q

Where do selectin molecules come form?

A
  • These are produced because mast cell and macrophages encounter microbes and secrete chemokines
  • Chemokines act on the endothelial cells and they starts to express E-selectin and ligands fro the L selectin to bind to the endothelial cells
31
Q

Where do they integrins come from? How do they work?

A

They slow down the leukocyte by forming lots of weak interaction with the endothelial cells
They are always expressed on the cells surface but normally have a low affinity
- Affinity is increased when it interacts with cytokines and ligands on the endothelial surface

32
Q

Why do integrins not always have high affinity?

A

This would cause the leukocyte to adhere to the capillary walls and it will not be able to be circulated

33
Q

How does the leukocyte migrate through the endothelium?

A

Has to pass 2 layers
1. Endothelial cells - Passes through via intercellular junctions (PECAM-1) and the leukocytes is pulled through
2. Basement membrane - leukocyte releases collagenase which breaks down the basement membrane

The enters extravascular space

34
Q

What is chemotaxis?

A

Once the leukocytes enters the cell the cytoskeleton will move it to the site of injury

35
Q

How do immune cells at inflammation site change over time?

A
  1. Starts with Neutrophils which are short living
  2. After 24hours it’s replaced by macrophages (live another 24 hours)
36
Q

How is inflammation stopped?

A

Once inflammatory stimuli is removed no more cytokines are released and no more leukocytes are being recruited
Stop signals are reasoned which stops this process e.g. TGF beta, IL-10

37
Q

What are the 5 outcomes of inflammation?

A
  1. Problem resolved
  2. Repair after tissue necrosis
  3. Abscess formation - puss released
  4. Immune response
  5. Chronic inflammation
38
Q

What are the 5 cardinal feature of inflammation?

A
  1. Redness - (rubor)
  2. Heat (calor)
  3. Swelling (tumor)
  4. Pain (dolor)
  5. Loss of function
39
Q

What are the 4 types of inflammation?

A
  1. Serous - fluid produced
  2. Fibrinous -
  3. Haemorrhagic - damage to blood vessels
  4. Purulent - pus-forming
40
Q

How is chronic inflammation distinguished from acute inflammation?

A
  1. Over a prolonged duration
  2. Tissue destruction
  3. Attempts of healing
41
Q

What causes chronic inflammation?

A
  • Persistent acute inflammation
  • Infection with certain microbs
  • Prolonged exposure to toxins
42
Q

What are the aims of wound repair and healing?

A
  1. Regeneration
  2. Repair
  3. Organisation
43
Q

What is regeneration?

A

Process where damaged tissue is replaced by similar cells

44
Q

What is repair?

A

Process where damaged tissue is replaced by fibrous scar tissue, this can cause a lose of function in some cases

45
Q

What is granulation tissue?

A

Mixture of new blood vessels and fibroblasts
- New blood vessels provide essential nutrients needed by growing cells or for repair
- Fibroblasts produce collagen needed for scar tissue

46
Q

What do fibroblasts do?

A

Produce collagen used to make scar tissue

47
Q

Stages of granulation?

A
  1. Extremely vascular
  2. Tissue undergoes remodelling until mature scar tissue is formed
48
Q

What factors effect healing and repair?

A
  1. Cell types involved e.g. stable?
  2. General factors e.g. age
  3. Local factors e.g. blood supply infection …
49
Q

What are complication of wound healing?

A
  1. Infection
  2. Wound breakdown
  3. Cysts formation - heals around and cyst can rupture
  4. Pain
  5. Weakness

Symposia (8 decks)

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