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Principles Of Pathology > Inflammation and healing > Flashcards

Inflammation and healing Flashcards

1
Q

How does a strep equi illicit an immune response?

A

Able to illicit a virus response through APC’s causing MHC class II mechanims to activate. https://s3.amazonaws.com/brainscape-prod/system/cm/173/281/304/a_image_thumb.png?1450543337

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2
Q

Can you describe the overall process of an acute inflammatory response involving all the leukocytes and cells?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/337/590/a_image_thumb.png?1450623701

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3
Q

Can you show how to distinguish between neutrophils, basophils, eosinophils and macrophages?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/337/010/a_image_thumb.png?1450622490

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4
Q

How can we test for strep equi?

A

qPCR test which will determine whether the horse is a carrier of the disease.

iELISA which is a serology test.

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5
Q

Describe the process of neutrophil emigration?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/337/421/a_image_thumb.png?1450623278

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6
Q

What are the vaccines for strep equi?

A

Equilis strep E- MSD/ a live attenuated vaccine intra lip admin. Cannot use alongside other vaccines not good for young horses

Pinnacle IN- Liver atten. Based on old strain not for new developing diseases.

Equivac 2 in 1- Highly immunogenic can easily conceive the disease.

Strangvac- best one multi virulent so especially good for bacteriophage.

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7
Q

How do you test for strangles?

A

Bacteria culture test. Which can also distinguish between s. zooepidemicus. Usually sugar fermentation.

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8
Q

What are dendritic cells?

A

They are present in almost all tissues, most numerous tissue exposed to the environment. Immature DCs take up the antigen and migrate to lymphoid organs to mature.

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9
Q

What is strangles caused by?

A

Streptococcus equi

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10
Q

How is strangles so successful and where does it “hide”?

A

Strep. equi hides in the right pharyngeal lymph node in the guttural pouch and can successfully be picked up by the nasal passage or saliva as seen in the picture: https://s3.amazonaws.com/brainscape-prod/system/cm/173/279/947/a_image_thumb.png?1450542900

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11
Q

What happens during phase 1 of wound healing?

A

Phase 1: Inflammation: There is clot formation which has immediate vasospasm, with platelet aggregation and release of vasoactive substances.

Inflammation part releases neutrophils, then predominantly macrophages and finally lymphocytes. Secretion of chemotactic growth factors also occurs

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12
Q

What are the different T cell subsets and the process from there?

A

TH1- Response to foreign body. APCs release IL-12. These commit CD4+ lymphocytes to the TH1 pathway. IL-2 increases proliferation of lymphocytes. IL-2+IFN(y) ilicit cytotoxic T cells response.

TH2- Allergic response. TH2 dendritic cells present antigen to TH cells, commiting TH cells to the TH2 pathway. TH2 release many interleukins. B lymphocytes produce anitbody response.

TH17- Induced by IL-23. Induces secretion of IL-17a. Involved in development of autoimmune responses. Predominantly on mucosal surface. Causes activation of neutrophils and other microbes.

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13
Q

What are the role of B lymphocytes in chronic inflammation?

A

The role of B lymphocytes is to be an antigen presenting cell. Differentiation into plasma cells. Plasma cells form in the lymph node mucosal surface etc. Resident plasma cells in bone marrow.

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14
Q

What are the main characteristics of acute inflammation?

A

Exudation of electrolytes, fluid, plasma,

Emigration of leukocytes ( from microvasculature)

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15
Q

Describe how macrophages are formed and there terms in the blood and other places etc?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/338/192/a_image_thumb.png?1450624818

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16
Q

What are the effector cells in chronic inflammation?

A

Dendritic Cells

Lymphocytes

T cells

B cells

Plasma Cells

Macrophages

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17
Q

What are the two different types of macrophages and how can they expressively be turned on?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/338/230/a_image_thumb.png?1450626269

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18
Q

Can you show all the inflammatory process cells?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/281/678/a_image_thumb.png?1450546274

19
Q

What are the subtypes of chronic inflammation?

A
  1. Lymphoplasmacytic
  2. Granulomatous
    a) Nodular
    b) Diffuse
    c) Eosinophilic
  3. Pyogranulomatous
20
Q

What are the hallmarks of inflammation under a microscope?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/337/608/a_image_thumb.png?1450623758

21
Q

What do mast cells do, what are they?

A

They are distrubuted through the connective tissue, near small blood and lymphatic vessels of skin and mucous membranes. Interact with dendritic cells and release mediators that activate endothelial cells.

Key features of mast cells is the granules due to histamine- eosinophilic.

22
Q

What are the 5 mechanisms leading to chronic inflammation?

A
  1. Persistance/Resistance
  2. Isolation
  3. Unresponsiveness
  4. Immune-mediated
  5. Leukocyte defects
  6. Unidentified
23
Q

What are granulomas and how are they formed?

A

They are caused and formed by necrotic centres. As a result H accumulation in response to pathogen. This is heterophilic. Histiocytic has remnants of macrophage aggregates which are stimulated by intracellular pathogens such as mycobacteria.

24
Q

What do avian and exotic species have in the blood that differentiates them to everyone else?

A

They have a nucleus in the red blood cells

25
Q

What is a multinucleate giant cell? (MNGC)

A

It is formed by the fusion of multiple macrophages and can be activated by stimulated cytokines, IL-3,4, IFN (y)

26
Q

What are neutrophils, when does their role play a part?

A

Neutrophils are the first types of leukocytes to be recruited in inflammatory exudate. Their function is to kill microbe- phagocytosis and kill tumour cells. They can also eliminate foreign material. And the infiltrate areas of necrosis.

27
Q

What can chronic strep equi cause?

A

Can form chondroids which are pus like material that can be described of a texture similar to cottage cheese. It is from accumulation of purulent material in the guttural pouch. These can be visible in carriers of strep equi.

28
Q

How does strep. equi cause a infect a host, is it a virus or a bacteria?

A

Bacteriophage waits until a POP and releases the virus inside. Essentially it is a bacteria with a host virus inside. The “bacteria” can they use reverse transcriptase to replicate inside the cell causing phage proliferation.

29
Q

How does the repair process actually work?

A

Granulation tissue is progressively replaced by fibrous tissue

decrease in leukocytes, oedma, vascularity etc.

increase in spindle shaped fibroblasts, dense collagen etc.

Fibroblasts proliferate due to TGF-b

Collagen synthesis due to TNF, IL-1, IL-4 etc.

30
Q

What are eosinophils?

A

Eosinophils are recruited in an allergic response. They are slightly larger than neutrophils. And contain specific granules. They are major basic protein.

31
Q

What is wound contraction and the technical term?

A

Scirrhous reaction= contraction of the connective tissues with tension on surrounding tissues.

Myofibroblasts- contractile fibroblasts

formed from tissue fibroblasts or fibrocytes

production mediated TGF-b

continous contractions

produce large amounts of ECM

32
Q

What is captive stress?

A

This is chronic stress which has been induced by a low grade state of inflammation. It is a mixture of neuro-endocrine and sympathetic stress that overall adds to the inflammatory process.

33
Q

Describe three things in an inflammed capillary bed?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/337/294/a_image_thumb.png?1450622962

34
Q

How do you manage a farm with strep equi?

A

Outbreak management can occur with the horses splitting them into three main groups, no contact, clinical signs and in contact with the clinical signs group.

This will allow the horses with contact to develop the disease to a stage where it is diagnosable.

Quarantine and screen for new horses coming in.

35
Q

What is acute inflammation?

A

It is a vasoconcentric response to a progressive reaction of vascularized tissue to injury over time. Usually a short duration lasting hours to days.

36
Q

What are lymphocytes?

A

They enter the site of inflammation 24-48 hours after initial site of lesion. Divided into T cells cell mediated or B cells humoral immunity. To distinguish use immunohistochemistry.

37
Q

Can you show how the body repairs after chronic inflammation or acute inflammation?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/339/338/a_image_thumb.png?1450626731

38
Q

What are NK cells?

A

NK cells enter the lesion hours after initiation. They kill target cells through release of perforin granules. There are two types of NK cells.

39
Q

What happens during phase 2 of wound healing?

A

Phase 2: Proliferation: Bridging of surface defects by epithelium. Degradation of surface matrix. Proliferation of new blood vessels. Remodelling of extracellular matrix. Fibrin, fibronectin etc.

40
Q

What are the different stages in wound healing, 3 main phases?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/339/364/a_image_thumb.png?1450626809

41
Q

How does fibrosis occur?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/340/046/a_image_thumb.png?1450628222

42
Q

What happens during phase 3 of wound healing?

A

Connective tissue remodelling. Degradation of collagen and ECM by collagenases. Replacement of type III with type 1 collagen wound contraction. Area of damage is replaced by mature fibrous tissue with abundant collagen.

43
Q

How can the body heal? Three main (steps)?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/339/287/a_image_thumb.png?1450626645

Principles Of Pathology (8 decks)

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