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Pathology > Inflammation and Phagocytosis > Flashcards

Inflammation and Phagocytosis Flashcards

1
Q

What is keratitis?

A

Inflammation of the CORNEA.

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2
Q

Define Inflammation…

A

A reaction of vascularized living tissues to injury.

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3
Q

What are characteristics of inflammation?

A

Inflammation involves Changes in vascular bed (epithelium), blood, and connective tissue. The intention of inflammation is to eliminate the irritant and repair the damaged tissue.

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4
Q

What are the 5 signs of inflammation? (Mainly acute inflammation)

A
  1. Redness
  2. Swelling
  3. Pain
  4. Loss of Function
  5. Heat
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5
Q

What are the roles of inflammation?

A
  1. Dilute, contain and isolate injury
  2. Destroy invading microorganisms and/or inactive toxins
  3. Achieve healing and repair
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6
Q

What are the outcomes of inflammation in ideal, intense and failed conditions?

A
  1. Ideal conditions - return to normal
  2. Intense inflammatory response - attempt to separate injured tissue
  3. Failure to eliminate insult - sequel/consequences
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7
Q

In intense inflammatory response, there is formation of WHAT?

A

Formation of a wall - like a capsule in an abscess - surrounded by fibrous connective tissue.

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8
Q

If there is failure to eliminate the insult during inflammation, WHAT forms?

A

A scar forms! Ex: chronic dermatitis - thickening of the dermis.

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9
Q

The inflammatory response requires WHAT in order to occur?

A

An initiating Stimulus (Etiology)!

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10
Q

True/False: Inflammation occurs in living and dead tissues.

A

False - only in LIVING tissues

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11
Q

True/False: Inflammation can be more harmful than the initial stimulus.

A

True.

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12
Q

True/False: Inflammation is fairly stereotyped/predictable irrespective of etiology.

A

True.

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13
Q

Through what components is Inflammation critically tied to the blood?

A

Through Plasma circulating cells, blood vessels, cellular and extracellular components.

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14
Q

When does inflammation end?

A

When the stimulus is eliminated.
Mediators are broken down and dissipated.
WBCs have short half-lives.

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15
Q

Define Exudation…(we need to know this!)

A

The escape of fluid, proteins and blood cells from the vascular system into the interstitial or body cavities.

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16
Q

Define Transudate…(we need to know this!)

A

An ultra filtrate of blood plasma and results from hydrostatic imbalances across the vascular endothelium.

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17
Q

Inflammatory extravascular fluid that has

high protein concentration, much cellular debris and a Specific Gravity above 1.020 is a…

A

EXUDATE!

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18
Q

Fluid with a low protein content and a specific gravity LESS than 1.020 is a…

A

TRANSUDATE!

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19
Q

Pyothorax is characterized by…exudate or transudate?

A

PUS..cloudy, whitish material within the thoracic cavity…this is an EXUDATE!

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20
Q

Define Edema…

A

An excess of fluid in the interstitial tissues or serous cavities. Can be either an exudate or a transudate!

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21
Q

When is Edema an exudate?

A

Inflammatory edema

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22
Q

Define Pus…

A

Inflammatory exudate rich in leukocytes and parenchymal cell debris.

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23
Q

What are the primary leukocytes in Pus?

A

Mainly neutrophils - viable and degenerated!

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24
Q

How do you classify Exudate?

A

Serous
Fibrinous - fibrin is the main component
Suppurative
Granulomatous - has a lot of macrophages

Duration - acute or chronic

see the table in the Inflammation lecture from 5.15.15

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25
Q

What does EXTENT mean when classifying exudate?

A

Extent mean How Bad is it?

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26
Q

“Greasy Pig Disease” is an example of…

A

Severe Exudative Dermatitis in a Pig

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27
Q

Describe the characteristics of Peracute Inflammation?

A

ex: Anaphylactic Shock
Usually caused by a potent stimulus.
Usually the animal has no time to respond.
It is less common than acute disease processes.

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28
Q

What are General Features of Peracute Inflammation?

A

Time: 0-4 hrs
Vascular Involvement: Hyperemia, Slight edema, and Hemorrhage
Inflammatory Cells: Not usually numerous, few leukocytes
Clinical Signs: Shock and Sudden Death

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29
Q

Give an example of Peracute Inflammation…What do you see Grossly and Histologically?

A

Infectious canine hepatitis
Grossly - congestion and edema of abdominal viscera
Histologically - intranuclear inclusions within glomeruli

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30
Q

Acute Inflammation Characteristics are…

A

Time: begins within 4-6 hrs
Vascular Involvement: Active hyperemia, edema and occasional fibrin thrombi within vessels (will occlude the vessel).
Inflammatory Cells: leukocyte infiltration is variable, NO MACROPHAGES! Mainly neutrophils.

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31
Q

What causes Edema in Acute Inflammation?

A

Edema in Acute Inflammation is due to endothelial damage - lymphatics and small blood vessels.

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32
Q

What is the role of lymphatics in Acute Inflammation?

A

Moving away the Exudate!

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33
Q

What is Lymphadenitis?

A

It is reactive inflammation of lymph nodes that occurs in acute, subacute, and chronic inflammation.

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34
Q

What is Lymphangitis?

A

Inflammation of lymphatic vessels.

ex: thickening of serial lymphatic vessels (chronic lymphangitis) due to Johne’s disease

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35
Q

Define Subacute Inflammation…

A

The gradual change between acute and chronic inflammation

Response DOES NOT include reparative responses like fibroplasia and angiogenesis.

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36
Q

What inflammatory cells do you see with Subacute Inflammation?

A

Inflammatory Cells will be “mixed” or “pleocellular” inflammatory infiltrate.
Primarily Neutrophils…may have lymphocytes macrophages and plasma cells.

37
Q

Chronic Inflammation

A

result of a persistent inflammatory stimulus in which the host has failed to completely eliminate the causative agent.

38
Q

Chronic Inflammation is characterized by evidence of 2 host tissue responses in terms of repair….What are they?

A
  1. Scar tissue formation!

2. Parenchymal Regeneration!

39
Q

What is the origin of Chronic Inflammation?

A

Follow an acute inflammatory phase

May develop as an insidious, low-grade, subclinical process without history…

40
Q

What is an example of Chronic Inflammation?

A

Multifocal ulcerative colitis, chronic in the feline
Chronic lymphangitis - Johne’s disease in the goat
See image from Lecture!

41
Q

What are the 5 Classifications for Distribution?

A

Focal, Multifocal, Coalescent, Locally extensive, Diffuse

42
Q

Define Focal Inflammation…What is the Size of a Focal Inflammatory Lesion?

A

SINGLE abnormality or inflamed area within a tissue

Size: varies from 1 mm to several centimeters in diameter

43
Q

What is the #1 rule when making an “Interpretation”?

A

COVER YOUR @$$!!!

44
Q

Define Multifocal…What is the Size of a Multifocal Inflammatory Lesion?

A

Arising from or pertaining to many foci
Size: Variable. Each focus of inflammation is separated from other inflamed foci by an intervening zone of relatively normal tissue.

45
Q

What is Multifocal to Coalescent?

A

It is an indication of severity.

46
Q

What is Locally Extensive classification?

A

Involves a considerable zone of tissue within an inflamed organ.
Origins: severe local runs that spread into adjacent normal tissue
Coalescence of foci in a multifocal rxn
Exxample: Cranioventral…
Locally extensive pneumonia in Pigs

47
Q

What are the characteristics of Diffuse Classifications of Inflammation/Lesions?

A

The entire tissue is involved. Ex: Interstitial pneumonia

Diffuse lesions are often viral or toxic in etiology.

48
Q

What is Exudate? What are the 3 Common Types?

A

Classification according to the type of inflammatory cells and exudate/fluid.
Common types: Suppurative (more common)
Fibrinous and Serous (watery-type fluid)

49
Q

What are the Classifications of Exudate? (7)

A

serous, supurative, fibrinous, serofibrinous, fibrino-purulent, purulent, granulomatous

50
Q

Suppurative Exudation

A

consisting of, or containing pus; associated with the formation of pus

51
Q

What is Pus? What is it composed of?

A

Pus is: A liquid inflammation product composed of…
accumulated dead cells
variable numbers of viable leukocytes (primarily neutrophils)
fluids added by the inflammatory edema-forming process

52
Q

What are some examples of Suppurative Exudate?

A

Suppurative bronchopneumonia in a dog. Local Infection!
Ex: Pyometra in a dog
Ex: Chronic Suppurative Osteomyelitis - neutrophils came into the bone marrow and destroyed the bone marrow and the bone! - It took a while! “Focal Suppurative Osteomyelitis”

53
Q

What is Suppuration?

A

The Process of Pus formation.

54
Q

What is an Abscess?

A

Circumscribed (partially walled-off) collection of pus.

Gross Appearance: yellow-to-white/gray and varies from watery to viscous depending on fluid content.

55
Q

Is an Abscess Suppurative Inflammation?

A

Yes!

56
Q

What is the Pathogenesis of Fibrinous Exudation?

A

Pathogenesis: severe injury to endothelium and basement membranes results in leakage of plasma proteins including fibrinogen, which polymerizes perivascularly as fibrin.

57
Q

What does fibrinogen do?

A

Once out of the blood vessel, it polymerizes perivascularly and forms Fibrin - Fibrin is the first step of Adhesion!

58
Q

What is the Gross Appearance of Fibrous Inflammation?

A

Gross Appearance: yellow-white, pale, tan stringy, shaggy meshwork - giving a rough irregular appearance to the tissue surfaces.
Fibrin Casts of friable materials may form in the lumen of tubular organs.

59
Q

Is the process of Fibrous Inflammation Chronic or Acute?

A

Acute Process - can form in SECONDS!

60
Q

Fibrinopurulent Exudate is a term…

A

used to classify an inflammatory process in which neutrophils and fibrin are abundant
ex: fibrinopurulent pericarditis in a foal

61
Q

Presence of a fibrinous exudate involves what kind of process?

A

AN ACUTE PROCESS!

62
Q

What kind of process is Fibrosis?

A

A CHRONIC PROCESS! - it is part of the scar tissue!

63
Q

What are the Functions of Fibrin…

A

Provides support for the eventual ingrowth of fibroblasts and neocapillaries - a process known as ORGANIZATION of the Exudate.
* *the transformation of the fibrinous exudate (acute process) into well-vascularized C.T. (chronic process - known as the ORGANIZATION of the exudate)

64
Q

How is Fibrin removed?

A

Enzymatic fibrinolysis or by phagocytosis by macrophages before organization can occur.

65
Q

Fibrinous Vs. Fibrous

A

MAKE SURE YOU KNOW THE DIFFERENCE! LEARN IT NOW!

66
Q

Serous Exudation

A

Inflammatory process in which the exudate occurs in tissues in the absence of a prominent cellular response.
May be a dominant pattern for a variety of mild injuries like Traumatic blisters, etc.

67
Q

Gross Appearance of Serous Exudation:

A

Yellow, straw-like color, fluid commonly seen in early stages of inflammatory responses. - - Ulceration follows the rupture of the vesicle.

68
Q

Granulomatous Inflammation is ALWAYS…

A

ALWAYS ALWAYS ALWAYS CHRONIC!

69
Q

Characteristic cells of Granulomatous Inflammation…

A

-characterized by predominantly macrophages as well as lymphocytes and plasma cells

70
Q

Large cells with abundant cytoplasm in a Granulomatous Inflammatory response are referred to as…

A

“multinucleate giant cells” or “epithelioid cells”

71
Q

How are the macrophages arranged in a Granulomatous Inflammatory response?

A

Macrophages are clustered in a characteristic elliptical formation around the causative etiologic agent, or around a central necrotic area, or simply as organized nodules

72
Q

Describe the Etiology of Granulomatous Inflammation…what Infectious Organisms are involved?

A

usually some non‐digestible organism or particle which serves as a chronic inflammatory stimulus, delayed‐type hypersensitivity is often required.
ORGANISMS:
• Mycobacterium, Actinomyces, Blastomyces,
Coccidioides, etc)

73
Q

What are the Non-Infectious Agents that could cause the Etiology for Granulomatous Inflammation?

A

Noninfectious AGENTS: Mineral oil, Complex polysaccharides, Foreign bodies

74
Q

What are other types of Inflammation modifiers? (3) What type of diagnosis are these used in?

A

Modifiers: Necrotizing, Hemorrhagic, Mucoid - - can be used in a morphologic diagnosis

75
Q

What is necrotizing Inflammation?

A

Necrosis is the main feature and exudation is minimal. In general, the is interpreted as inflammatory (rather than purely ischemic) if an infectious etiology is suspected.

76
Q

What is Hemorrhagic Inflammation?

A

Hemorrhage is the main feature of this type of inflammation. The presence of an etiologic agent will indicate that the process is inflammatory rather than a primary circulatory disturbance.

77
Q

Describe the Inflammatory exudate in Mucopurulent or Catarrhal Inflammation?

A

The inflammatory exudate is composed of mucus and pus (neutrophils and cell debris).

78
Q

List the Chemical Mediators of Inflammation…

A 
• Vasoactive amines
• Plasma proteases: complement
• Lipid mediators such as arachidonic
acid
• Platelet activating factor (PAF)
• Cytokines
• Chemokines
• Nitric Oxide (NO)
79
Q

What are the events of Acute Inflammation?

A
  1. Stimuli for onset of acuteinflammation
  2. Vascular changes
  3. Cellular events
  4. Termination of acute inflammatory response
80
Q

Define Extravasation…

A

extravasation= delivery of white blood cells to the site of injury

81
Q

What are the Events of Extravasation?

A
  1. Margination (tethering)
  2. Rolling
  3. Activation and Adhesion
  4. Transmigration
82
Q

What bovine (and canine) disease is due to leucocyte adhesion’s failure? Etiology?

A

Leucocyte Adhesion Deficiency (LAD)

Etiology: Type 1 Mutation in Beta-1 Integrins CD18

83
Q

What is the mechanism of LAD?

A

neutrophilia with impaired transmigration because neutrophils are unable to adhere

84
Q

What are the Clinical Signs of LAD?

A

Clinical signs: gingivitis, tooth loss, ulcers in oral and enteric mucosa, cutaneous ulcers, pneumonia

85
Q

Define Chemotaxis…

A

the process where white blood cells emigrate in tissues toward the site of injury

86
Q

What are the 3 Interconnected Processes of Phagocytosis?

A

– Recognition and attachment of the particle to be ingested
– Engulfment with subsequent formation of phagocytic vacuole
– Killing or degradation of the ingested material

87
Q

How do you terminate the acute inflammatory response?

A

Degradation of inflammatory mediators.

Production of Stop Signals after the stimulus has been removed.

88
Q

What do the Inflammatory Stop Signals do?

A

– Switch from pro‐inflammatory leukotrienes to anti‐
inflammatory lipoxins from arachidonic acid
– Liberation of anti‐inflammatory cytokines such as TGF‐ beta from macrophages and other cells.
– Neural impulses resulting in inhibition of TNF production in macrophages

Pathology (14 decks)

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