Pathology Of Inflammation Flashcards

1
Q

What are the differences between exudate and transudate?

A

Exudate is fluid that is rich in proteins or cells and contain fibrinogen —> fibrin mesh

Transudate fluid that contains no proteins (normally due to high hydrostatic pressure)

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2
Q

Typical features of acute inflammation

A

Short lived neutrophil rich

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3
Q

Typical features of chronic inflammation

A

Long lived and is lymphocyte and macrophage rich

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4
Q

What are the differences between cell-derived inflammatory mediators and plasma derived inflammatory mediators

A

Cell derived are form platelets, mast cells and and other inflammatory cells that release various chemicals
Platelets —> serotonin
Mast cells —> histamine
Inflammatory cells —> lymphokines and monokines

Plasma derived consists of the
Complement system
Fibrinolytic system and coagulation system
Kinin system

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5
Q

What releases PAF and what is the role of PAF in acute inflammation

A

Cells such as monocytes, macrophages, basophils and mast cells release PAF which causes platelet aggregation. This activates the arachidonic acid pathway that leads to production of prostaglandins + thromboxanes and leukotrienes

PAF can modify permeability of endothelial cells by changing adhesion of polymorphs

  • macrophages can be activate by PAF to release more PAF or can also secrete PAF
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6
Q

What are the two pathways of arachidonic acid

A

Cycloxygenase pathway that produces prostaglandins = pain perception and vasodilation
Prostacyclin - inactivate platelets
Thromboxane - vasoconstriction and platelet aggregation

Lipo -oxygenase pathway that produces various forms of leukotrienes
LTB4 = chemotaxis and neutrophil adhesion

LTC4, LTD4, LTE4 = increased vascular permeability and vasoconstriction

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7
Q

What are acute phase reactions

A

Increase in leucocyte production, fever, decrease in blood pressure, and appetite and tachycardia

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8
Q

What are other systemic effects of acute inflammation

A

Pyrogens such as IL-1 and IL-6 can be released (endogenous pyrogen)
Altered liver metabolism of acute phase proteins
HPA axis is altered which leads to metabolic changes and this feeling of malaise

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9
Q

What is resolution?

A

Restoration of normal tissue when architecture is still intact. (If this is not possible then repair occurs)

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10
Q

What is organisation?

A

Scar formation due to loss of structural integrity

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11
Q

An example of long term persistent acute inflammation is an absess

A

Accumulation of neutrophils and is walled off by fibrin mesh so environment remain neutrophil rich
Other inflammatory cells may be present

*formation of an absess is an example of suppurative inflammation

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12
Q

Types of chronic inflammation

A
  • non specific = characterised by plasma cells and lymphocytes. Normally supervenes after a bacterial or viral infection
  • chronic suppurative eg osteomyelitis
    If eosinophil rich indicates parasitic infection
  • granulomatous inflammation = doesn’t start with acute inflammation. Normally a response to agents which are hard to get rid of. Formation of giant cells
  • autoimmune = antibodies such as IgM and IgG against body’s own cells
    Plasma cells
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13
Q

Resolution is archived through which metabolites:

A

Resolvins, protectins and lipoxins

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14
Q

TB granuloma

A

Caseating granuloma

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15
Q

Sarcoid granuloma

A

Non-caseating granuloma

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16
Q

Basis of immunostaining

A

Use of antibodies against certain types of molecules or cells

17
Q

Intracellular-vital fluorescent microscopy

A

Use to see whether cells or molecules are mobile in a granuloma for example

18
Q

Examples of non-invasive imaging

A

MRI
FFPE sections can yield molecular information