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VET375 Pathology > Immunity and Inflammation > Flashcards

Immunity and Inflammation Flashcards

1
Q

List the major components of the innate and adaptive arms of the immune system ?

A
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2
Q

Where do T cells require further maturation ?

What cells leave the bone marrow , as mature cells ?

A
  1. Thymus
  2. Myeloid cells, B cells and NK cells
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3
Q

List 2 patterns which occur in tissues by conserved microbial components shared by many pathogens ?

A

PAMP - pathogen associated molecular patterns

DAMP - danger associated molecular patterns

they bind to PRR pattern recognition receptors, expressed on all myeloid cells.

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4
Q
  1. What PAMP , which is found on gram -ve bacteria, which macrophages are very responsive to ?
  2. What is the PRR on the macrophage that this PAMP binds to ?
  3. What are the cytokines expressed when these two bind together ?
A
  1. Lipopolysaccharides (LPS)
  2. TLR4
  3. IL-B, IL-6, TNFa
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5
Q
  1. Where are naive lymphocytes (T&B cells) activated?
  2. They are activated by a specific antigen presented to the cell, for T & B cells what is the receptor?
A
  1. lymphnodes
  2. Tcell = TCR . B cell = BCR (they will not respond to anything else)
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6
Q

After activation of naive lymphocytes, how long does it last for;

  1. clonal expansion
  2. effector lymphocytes
  3. memory lymphocytes
A
  1. 10-14 days after 1st exposure
  2. days - weeks
  3. weeks, months & years
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7
Q

What is the function of ;

  1. B lymphocyte
  2. Helper T lymphocyte
  3. Cytotoxic T lymphocyte
  4. Regulatory T lymphocyte
  5. Natural Killer Cells
A
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8
Q
  1. Define the term antigen , and
  2. The roles of antigen presenting cells in T cell activation ?
  3. What are the 3 major APC ?
A
  1. Antigen = any substance that can stimulate anti body generation.
  2. APC (antigen presenting cells) process antigens by TCR & BCR
  3. Dendritic cells, macrophages & B cells
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9
Q
  1. What Major Histocompatibility Compex (MHC) is expressed on all nucleated cells?
  2. Where is the other class expressed?
A
  1. MHC class 1
  2. Class 2 are expressed only on specialised APC, eg dendrenic cells
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10
Q
  1. CD8+ TCR can only bind to , what MHC Clas
  2. What functio to T cells gain when activated by CD8?
A
  1. MHC Class 1
  2. They become cytotoxic T lymphocytes., which kill virally infected cells.
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11
Q
  1. What Class can CD4+ TCR recognise ?
  2. What role does an activated CD4 + T cell have ?
A
  1. MHC Class 2
  2. Helps B cells make antibodies and can amplify CTL responses.
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12
Q

What cytokine induces the subset of the following CD4 + T cells ?

A
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13
Q
  1. Who does CD4 + T cells help to make long lived high-affinity antibodies ?
  2. What does CD4 + T cells also provide?
  3. What do they signal ?
A
  1. B Cells that have recognised the same antigen
  2. They also provide growth factors (cytokines)
  3. Help B cells for affinity, maturation and isotope switching.
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14
Q

State the major types of immunopathologies?

Their causes

Their consequences

A
  1. Insufficienct of the immune response
    1. Inherited and acquired immunodeficiencies
    2. Over-activity of the immune response
      1. Hypersensitivies & allergies
    3. Disruptions to self tolerance
      1. autoimmune diseases
    4. Neoplasias of the immune system
      1. Lymphomas and leukemias
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15
Q
  1. What are the different types of hypersensitivities?
  2. What are the mechanisms of type 1 ?
A

Type 1 - IgE mediated mast cell degranulation

Type 2 - IgG medicated cellular toxicity

Type 3 - Immune complex mediated (IgG, IgM)

Type 4 - T cell mediated (CD4 or CD8) ; delayed type (DTH)

2.

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16
Q

What is the concept of self -tolerance and its major mechanisms ?

A

Self tolernace is required to avoid damaging self directed immune reponses - central and peripheral tolerance

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17
Q

Exlpain how disruption of self - tolerance leads to autoimmune disease?

A
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18
Q

What is acute inflammation and its cardinal signs ?

A

Rapid & Local response to limit tissue damage due to injury.

Primarily an innate response

Cardinal Signs

Heat (calor)

Pain ( dolor)

Redness ( rubor)

Swelling ( tumor)

Loss of function

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19
Q

What are some inducers of acute inflammation ?

A
  • infections
  • trauma (+/- sterile)
  • physical and chemical agents
  • foreign bodies
  • tissue necrosis (bad death)
  • hypersensitivity reactions
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20
Q

What are the 4 components of Acute inflammation ?

A
  1. Vascular response
    1. changes to blood flow and vessel permeability
    2. Cellular response
      1. recuritment of leukocytes
    3. Solubale mediators
      1. co-ordinators of the tissue response
    4. Molecular “sensors”
      1. control the type of inflammation
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21
Q

What are the 5 key processes of the vascular response

A
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22
Q

What are the mechanisms of increased vascular permeability ?

A
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23
Q

Explain the sequence of events and key molecules involved in leukocyte extravasation?

A
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24
Q

Describe the main types of cells an molecules inovlved in the cellular response?

A
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25
Q

What is the key function of a neutrophil ?

Its role in acute inflammation ?

A
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26
Q

What is the key function of a eosinophil ?

Its role in acute inflammation ?

A
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27
Q

What is the key function of a Mast Cells ?

Its role in acute inflammation ?

A
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28
Q

Where are Monocytes and Macrophages found?

Its role in acute inflammation ?

What do they produce?

What can they form?

A
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29
Q

What are the key functions of Lymphocytes

A
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30
Q

Explain the Cellular process of Phagocytosis

What Cells are ablt to perform it

A
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31
Q

Explain the Cellular process of Chemotaxis

A
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32
Q

What cells are respond to the following:-

  • Bacteria
  • Viruses
  • Parasites
  • Allergens
A
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33
Q
A
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34
Q

Why are soulable mediators important in Accute Inflammation?

A
35
Q
  1. What initiates all four plasma protein cascade systems?
  2. What are the four systems?
A
  1. Activated Hageman Factor (Factor XII)
  2. Kinin Cascade, Clotting system, Fibrinolytic System, Complement System
36
Q

What is the Kinin Cascade.

What activates it?

Kallikren itself is a potent activator of what?

A
37
Q

What is the main link between the Coagulation systme and Inflammation?

A
38
Q

What is the main function of the cell derived mediator - Histamine

When is Histamine released and from where?

A
39
Q

What is the main function of the cell derived mediator - Eicosanoids (Arachidonic Acid Metabolites

A
40
Q
  1. What are Cytokines also known as?
  2. What do Cytokines activate and what produces them?
  3. What are their major actions?
  4. Which ones play a major role in Acute Inflammation?
A

Also known as interleukins (IL)
• Small molecular weight protein messengers
• Activate leukocytes and are produced by leukocytes
after activation
• Can act locally or at long distances (systemically)
• Major actions
– Endothelial activation
– Leukocyte activation
– Fibroblast recruitment
– Priming of neutrophils
– Differentiation of lymphocyte subsets
• IL-1, IL-6 and TNF alpha play major roles in AI

41
Q

What are some of the main actions of cytokines and their roles in the acute phase response?

A
42
Q

What are the possible outcomes of Acute Inflammation?

A

Outcomes of Acute Inflammation

  1. Complete resolution
  2. Healing via fibrosis
  3. Progression to chronic inflammation
  4. Excessive tissue damage (pathology)
43
Q

What are the affected sites that these clinical terms relate to?

A

Stomatitis (mucositis) - Mouth/oral cavity
Laryngitis - Larynx
Glossitis - Tongue
Otitis- Ear
Dermatitis - Skin
Myocarditis - Heart
Pericarditis - Pericardium
Pancreatitis - Pancreas
Insulitis - Islets of Langerhans
Uveitis - Uvea/choroid (eye)
Encephalitis - Brain
Gastritis - Stomach
Pneumonitis (pneumonia) - Lung
Pleuritis (pleurisy) - Pleura
Thyroiditis - Thyroid gland

44
Q

What are the possible outcomes of acute inflammation?

A
45
Q

Relate the following Terminology to inflammation

  1. Transudate
  2. Modified Transudate
  3. Oedema
  4. Exudates
  5. Effusion
A
46
Q

What is a Sero-Sanguineous Exudate/Effusion.

When it is in the lungs what is a result of?

A
47
Q

What are some of the Inflammatory Exudates?

A

• Serous
• Sero-saguinous
• Fibrinous
• Sero-fibrinous
• Purulent/Suppurative
- Mucopurulent
- Abscess
• Haemorrhagic
• Diptheritic
• Ulcer
Can provide clues about the underlying cause of the disease

48
Q

What is a Serous Exudate/Effusion?

What colour does it stain with H&E?

What is its main purpose?

A
49
Q

What is a Fibrinous Exudate/Effusion?

A
50
Q

What is a sero-fibrinous exudate/effusion?

What can it be characteristic of?

A
51
Q

What is a Purulent Exudate/effusion?

What is it comprised of?

What colour would you expect it to be?

What is it indicative of?

A
52
Q

What is an abscess?

Why do they appear?

How do they heal?

A
53
Q

What is a Haemorragic Exudate/Effusion?

A
54
Q

What is a Diptheritic Exudate?

Where would they usually occur??

A
55
Q

What is an Ulceration?

Where are they usually found?

What can cause Gasteric Ulcers?

A

Gastric Ulcers are caused by NSAIDs and Helicobacter Pylori

56
Q

The Cellular Response

Bacteria

Viruses

Allergens

Parasites

A
57
Q

What are the cell derived soluble mediators for:-

  • Arachidonic Acid Metabolites
  • Vasoactive Amines
  • Cytokines and Chemokines
A
58
Q

What are the events in the resolution of inflammation?

A
59
Q

What are the 3 possible outcomes of Injury (Healing and Repair)

A

Outcomes of injury
1. The injury overwhelms the patient and
they die
2. The acute inflammatory response
removes the injured tissue and any
noxious agent, then the tissue heals.
3. The acute inflammatory response fails to
remove the injured tissue or a noxious
agent persists, then the inflammation
becomes chronic.

60
Q

What determines whether a tissue will regenerate or repair?

A

i. Cellular factors
ii. Chemical mediators: Growth factors
iii. Stromal factors: ECM
iv. Additional factors

61
Q

There are 3 classifications of cells by proliferative potential. What are they and where are they likely to be found?

A
  • Labile cells: most epithelial cells &

haematopoietic cells.

  • Stable cells: mesenchymal cells,

parenchymal cells. Cells are in G0 but can be
stimulated to return to G1.

  • Permanent cells: cardiac myocytes, neurons

(skeletal muscle). Cells have left the cell
cycle.

62
Q

There are 2 kinds of Stem cells what are they? And of the later one where are they found?

A

Stem Cells
1. Embryonic stem cells: 32
cell stage; Pluripotential;
asymmetric replication
2. Adult stem cells:
• bone marrow-haematopoietic
(HSC), progenitor & stromal); broad differentiation
potential;
• tissue stem cells: located in niches within most organ systems; Multipotent adult progenitor cells (MAPCS)

63
Q

What are the Essential Cellular elements of Healing?

A

Essential cellular elements of healing
Macrophages
Pivotal role- initiation and amplification of acute
inflammation AND progression of chronic inflammation and the transition between
inflammation and wound healing.
- Essential role in phagocytic removal of dead cells and matrix.
- growth factors necessary to the wound healing process eg PDGF, FGF, TGF a & b, VEGF
etc.

Fibroblasts
• main cell type in connective tissue;
• stable cells
• essential to wound repair:
• ECM components: eg collagen, fibronectin
structural integrity and tensile strength in wounds.
• Growth factors eg keratinocyte growth factor,
IGF-1.
• heterogeneous: some become contractile (myofibroblasts) - critical in wound contraction.

Endothelial cells
• respond early to growth factors such as VEGF (from macrophages, epithelium) at the site of tissue injury.
• a source of important growth factors (PDGF).
•early proliferation –> restoration of blood supply to the damaged tissue,
• Newly formed blood vessels = very leaky, releasing fluid –>nutrients and also proteins (eg
Ab, complement proteins) and cells important in the immune response.

64
Q

What are the signalling mechanisms used in cell growth (Healing and Repair)

A
65
Q

What are the 7 basic steps in Tissue repair?

A

Healing by repair is the restoration of damaged
tissue by regeneration and scaring.
Repair involves 7 basic steps:
1. Inflammation in response to tissue injury, with
removal of damaged and dead tissue
2. Proliferation and migration of parenchymal and
CT cells
3. Angiogenesis & granulation tissue formation
4. Synthesis of ECM proteins and collagen
5. Tissue remodelling
6. Wound contraction
7. Acquisition of wound strength

66
Q

What are some factors that can affect tissue repair?

A
  • continued tissue damage by the original agent or a secondary agent - especially bacterial infections and foreign bodies (local);
  • poor nutrition - particularly protein, Vitamin A, Vitamin C, Zn (systemic);
  • poor blood supply in the area - this varies from organ to organ (systemic or local);
  • metabolic disturbances e.g. diabetes, hyperadrenocorticism (systemic);
  • low temperatures (local or systemic);
  • low immune status (systemic).
  • Mechanical factors (local)
67
Q

What are the 2 types of Healing?

What are the four stages of Healing?

A

Primary (regeneration and repair - typicall of surgical incisions in skin)

Secondary (Occurs in wounds with seperatred edges)

The 4 stages of healing are :-

  • Inflammation
  • Granulation tissue formation
  • Wound Contraction
  • Remodelling
68
Q

Explain the timeframe of healing by Primary Intention

A
  • Activation of Haemostatis
  • Formation of the fibrin clot
  • activation of the inflammatory response
    • Within 24hours Neutrophils appear at incision margins and surface epithelium begiun to proliferate
    • within 36hrs Neutrophils are replace by macrophages
  • Day 3 - Granulation tissue begins to invade the incision space FGF2 and VEGF from macrophages, keratinocytes and endothelial cells promote angiogenesis
  • Day 5 - Incisional space is filled with granulation tissue, collegen fibres become abundant and begin to bridge the incisions (type III)
  • Day 7 wound strenght is 10% of unwounded skin
  • WOUND CONTRACTION - is achieved by formation of myofibroblasts within the granulation tissue (TGF-B increaseing tissue tension)
    • By the end of the 1st month a scar replaces the incision, composed of cellular connective tissue covered by intact epidermis
  • REMODELLING - During the first 2 months of healing collagen synthesis exceeds collagen degration, resulting in tensile strenght of heald skin approaching 70-80% of non wounded sking *type III prelaced by type I)
69
Q

What are the 3 general categories of Complications in skin wound healing?

A

3 General categories:

Deficient scar tissue formation

i. Wound dehiscence: mechanical stresses
ii. Ulceration: deficient blood supply

Excessive formation of the repair components

i. Proud flesh: Excessive granulation tissue
ii. Hypertrophic scar/ Keloid: XS collagen/ XS scar tissue
iii. Desmoids: exuberant fibroblast proliferation

Formation of contractures

I. Deformities of the wound +/- surrounding tissue

70
Q

What are some examples of chronic inflamation

A
  • Abscess Formation
  • Foreign Body Reaction
  • Chronic Trauma
  • Immune Mediated Chronic Inflammation
  • Granulomatous Inflammation
71
Q

What are the hallmarks of Chronic Inflammation?

A
  1. Cellular infiltrate comprises of any of :-
    • Macrophages
    • Lymphocytes
    • Plasma Cells (lesion > 2 weeks)
    • +/- neutrophiles / eosinophils
  2. The infiltrate destroys and replaces tissue
  3. Attempts at healing result in proliferation of tissue stroma and abundant fibrosis
72
Q

Chronic inflammation is always incited by the persistent presence of one of 4 things

A
  • An irritant (endogenous or exogenous) eg silica/ other foreign body
  • Micro-organism eg mycobacteria, fungi, parasites, viruses, OIA
  • Injured Tissue
  • An immune response (hypersensitivity and autoimmune diseases)
73
Q

What are some key features of a microbial abscess

A
  1. Persistent inciting agent (bacteria/fungi)
  2. Acute inflammatory response (neutrophils) fails to kill the micro-organism
  3. Central necrotic debris (purelent exudate) surrounded by a zone of macrophages/lymphocytes/plasma cells and encapsulated by fibrous tissue (walled off)
74
Q

What are the possible sequelae to an abscess?

A
  1. Micro-organism is killed - the abscess is organised (replaced by scar tissue) and becomes a cold abscess
  2. Bacteria proliferate, purulent exudate accumulates. Pressure builds up within the abscess, which then ruptures along the path of least resistance.
75
Q

Where are the 2 areas that an abscess may rupture?

A
  • External Rupture
    • ​Cavity, draining sinus/fistula fills with granulation tissue and heals by 2nd intention
  • Internal Rupture
    • ​Spread along fascial planes widespread fasciitis/cellulitis. Rupture into a blood vessel or airway.
76
Q

Chronic inflammation is classified based on the predominant cell type. Name the classification from these cell types

  • Macrophage
  • Epitheloid Macrophages and MNGC
  • Lymphocytes
  • Plasma Cells
  • Lymphocytes and Plasma Cells
  • Neutrophils and Epitheloid macrophages
A
  • Macrophage = Histiocytic
  • Epitheloid Macrophages and MNGC = Granulomatous
  • Lymphocytes = Lymphocytic
  • Plasma Cells = Plasmacytic
  • Lymphocytes and Plasma Cells = Lymphoplasmacytic
  • Neutrophils and Epitheloid macrophages = Pyogranulomatous
77
Q
  1. What is a Sequestrum
  2. What is a Involucrum
A
  1. Sequestrum = Necrotic bone acts as a foreign body
  2. Involucrum = Subperiosteal new bone covers the sequestrum
78
Q
  1. What is Granulomatous inflammation?
  2. What is a common disease which is a granulomatous inflammation?
A
  1. Characterized by predominately epithelioid macrophages +/- multinucleate giant cells as either a diffuse or nodular infiltrate.

Often occurs due to:

  • relatively inert foreign body,
  • intracellular/ indigestible micro-organisms
  • or, induction of a type IV hypersensitivity reaction
  1. Johne’s disease (Crohns disease) [Lamina propria is expanded by epithelioid macrophades filled with acid-fast bacteria, many lymphocytes and few plasma cells.
79
Q

What is the pathogenesis of Tuberculosis

A
80
Q

When a Cells is at G0 what kind of cell is it

A

Stable Cell (eg Hepatocyte)

81
Q

What are some factors which can affect tissue repair?

A
  • continued tissue damage
  • Nutrition
  • blood supply
  • metabolic disturbances
  • temperatures
  • low immune status
  • Mechanical factors
82
Q

What are the important cellular elements of chronic inflammation?

A
83
Q
  1. What is Septicemia?
  2. What is Bacteraemia?
A
  1. Bacteremia is the simple presence of bacteria in the blood while Septicemia is the presence and multiplication of bacteria in the blood. Septicemia is also known as blood poisoning.
  2. Septicemia is much more dangerous

VET375 Pathology (6 decks)

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