Lecture 10 2/16/24 Flashcards

1
Q

What leads to exudate?

A

accumulation of edema fluid, fibrin, and neutrophils in the extracellular space

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2
Q

Which cause of edema leads to exudate?

A

increased vascular permeability/inflammation

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3
Q

What are the characteristics of exudate?

A

-high protein conc.
-lots of cells and debris
-high specific gravity
-cloudy appearance

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4
Q

How does vasculitis differ from vascular permeability?

A

-vasculitis is an inflammatory response that targets the wall of the blood vessel
-vascular permeability is not associated with damage to the vessel

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5
Q

What is chemotaxis?

A

migration of leukocytes to the site of injury following a concentration gradient of chemokines and chemoattractants

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6
Q

Which chemokines are important for chemotaxis?

A

-IL-8: neutrophils/leukocytes
-IL-16: CD4+ T cells
-IL-17: monocytes/neutrophils
-chemerin: DCs and macrophages

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7
Q

What role does the leukotriene LTB4 play in chemotaxis?

A

-made by neutrophils
-recruits more neutrophils and macrophages

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8
Q

What are the characteristics of phagocytosis?

A

-carried out by neutrophils and macrophages
-cells eat organisms and cellular/necrotic debris
-specific process involving recognition, attachment, and opsonins

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9
Q

What are the general steps of phagocytosis?

A

-recognition and attachment
-engulfment
-killing and degradation

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10
Q

What are the effects of sloppy phagocytosis?

A

cell death and degradation of extracellular matrix due to intracellular/extracellular release of lysosomal enzymes

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11
Q

What are the characteristics of serous inflammation?

A

-leakage/accumulation of fluid with low plasma protein and no/few leukocytes
-practically transudates
-seen with thermal injury to skin and acute allergic responses

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12
Q

What are the characteristics of catarrhal inflammation?

A

-secretion/accumulation of thick, gelatinous fluid containing abundant mucus/mucins
-occurs in tissue with abundant goblet cells/mucous glands
-seen with chronic allergic and autoimmune disease

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13
Q

What are the characteristics of fibrinous inflammation?

A

-accumulation of fluid with high plasma proteins and no to few leukocytes
-lots of fibrin
-primarily on serous membranes of body cavities
-due to increased vascular permeability
-can be infectious or non-infectious in cause

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14
Q

What are the characteristics of fibrinous/fibrinonecrotic inflammation?

A

-fibrin covering an ulcer
-plaque of fibrin, neutrophils, and necrotic material
-typically on mucosal surfaces

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15
Q

What are the characteristics of hemorrhagic inflammation?

A

-involves hemorrhage
-often seen with necrosis (necrohemorrhagic)
-necrosis erodes blood vessels

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16
Q

How does hemorrhage differ from hemorrhagic inflammation?

A

-hemorrhage simply involves damage to blood vessel and blood leaking into tissues
-hemorrhagic inflammation is due to triggering of immune response and is often associated with necrosis of tissue

17
Q

What are the characteristics of necrotizing inflammation?

A

-involves necrosis
-usually in response to physical trauma
-can be fibrinonecrotizing or necrohemorrhagic

18
Q

How does necrosis differ from necrotizing inflammation?

A

-necrosis is simply cell death due to a variety of causes
-necrotizing inflammation involves necrosis and inflammation, with vessel damage leading to fibrin and blood leakage

19
Q

What are the characteristics of suppurative/neutrophilic/pyo-inflammation?

A

-accumulation of fluid with high conc. of plasma protein and high numbers of leukocytes/neutrophils
-usually in response to bacteria
-pus/purulent
-can be mixed with fibrin or necrosis

20
Q

How does suppurative differ from neutrophilic?

A

-suppurative occurs when pus has formed, causing tissue destruction
-neutrophilic is when neutrophils are just “hanging” out” in tissues

21
Q

Why do avian/exotic species with heterophils not have suppurate/pus-associated inflammation?

A

-lack myeloperoxidase
-do not liquefy exudate

22
Q

Which steps of inflammation lead to serous, fibrinous, hemorrhagic, or necrotizing inflammation?

A

-initiation
-vasodilation
-increased vascular permeability

23
Q

Which steps of inflammation lead to suppurative inflammation?

A

-activation of leukocytes
-diapedesis
-chemotaxis
-phagocytosis

24
Q

Which types of inflammation occur with a mix of all steps of inflammation?

A

-fibrinosuppurative
-necrosuppurative
-necrohemorrhagic

25
Q

What are the potential next steps following acute inflammation?

A

-resolution
-progression to chronic inflammation
-healing/repair

26
Q

What occurs during resolution?

A

-removal of inciting agent
-neutralization of inflamm. mediators
-return of vascular integrity
-leukocytes stop transmigrating
-apoptosis of neutrophils
-removal of edema fluid/leukocytes/foreign material/necrotic debris by macrophages and lymphatic system

27
Q

Which type of agents lead to resolution?

A

short-lived, rapidly decayed agents

28
Q

What is an abscess?

A

a circumscribed collection of pus with marked neutrophilic response

29
Q

What is important about the fibrous capsule surrounding an abscess?

A

indicates chronicity