Exam 3: Chronic Inflammation and Repair Flashcards

1
Q

What are the characteristics of chronic inflammation?

A

Predominance of mononuclear cells –> mainly macrophages, lymphocytes, and plasma cells
Vascular changes are minimal
Increased connective tissue (fibrosis)
Alteration in tissue architecture

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2
Q

Why does chronic inflammation occur?

A

Neutrophils are short lived
Neutrophils signal macrophages
Macrophages are longer lived –> can proliferate in tissues
Persistence of antigen
Some stimuli signal chronic inflammatory cells directly

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3
Q

When does an abscess develop?

A

When acute inflammation fails to eliminate stimulus

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4
Q

What is an abscess?

A

Liquefaction due to neutrophil enzymes

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5
Q

What does the color of exudate in an abscess depend on?

A

Pigment produced by inciting stimulus

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6
Q

What happens around exudate to form an abscess?

A

Fibroblasts produce collagen and form a thin connective tissue, which can mature into a fibrous capsule which eventually walls off

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7
Q

What is the inner wall of an abscess?

A

Granulation tissue: “pyogenic membrane”

Full of vessels that allow continual recruitment of neutrophils

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8
Q

Describe NAG

A

Grossly abscess and granulomas can be very similar in appearance. Sometimes abscesses can have thicker capsules but it depends on duration
Neoplasms can also be similar grossly
Differentials are Neoplasia, Abscess, and Granuloma (NAG)

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9
Q

Describe macrophages

A

Have abundant cytoplasm, can be foamy

Large, round nucleus that is sometimes indented

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10
Q

What does granulomatous mean?

A

Macrophages

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11
Q

What is granulomatous inflammation dependent upon?

A

Presence of indigestible organisms/particles

Presence of cell mediated immunity to inciting agent

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12
Q

What is seen grossly with granulomatous inflammation?

A

DIffuse: tissue appears thickened
Nodules: firm nodules of various sizes

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13
Q

What is seen microscopically with granulomatous inflammation?

A

Numerous macrophages present

Often accompanied by variable numbers of lymphocytes and plasma cells and connective tissue

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14
Q

What is the effect of granulomatous inflammation?

A

Chronic infection which the body cannot eliminate

Interfere with organ function

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15
Q

What are causes of granulomatous inflammation?

A

Bacteria
Fungi
Parasitic disease
Foreign bodes

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16
Q

What are bacteria and fungi resistant to that allows them to cause granulomatous inflammation?

A

Phagocytosis

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17
Q

What does the look of macrophages depend on?

A

Differentiation status

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18
Q

What are epithelioid macrophages?

A

Abundant eosinophilic cytoplasm and large pale nuclei

More secretory and less phagocytic than typical macrophages

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19
Q

What are giant cells?

A

Large, multinucleated cells that arise from the fusion of macrophages

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20
Q

What is a granuloma?

A

Macrophages that are in aggregates

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21
Q

Describe classic granulomas

A

Central core of caseous necrosis
Zone of epithelioid macrophages and giant cells
Zone of lymphocytes
An outer zone of fibroblasts and fibrosis

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22
Q

How can you differentiate between diffuse and nodular granulomatous inflammation?

A

Morphologic forms based on immunologic response
Th2–> diffuse granulomatous inflammation
Th1–> nodular granulomas

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23
Q

What is a stage 1 granuloma?

A

Days after infection

The lesion site is infiltrated by neutrophils, monocytes, macrophages, and lymphocytes. Epithelioid macrophages form

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24
Q

What is a stage 2 granuloma?

A

From roughly 48 hours to multiple days and weeks
Lesions contain macrophages, epithelioid macrophages, thin rims of fibrous connective tissue, variable numbers of lymphocytes, MGCs can also form

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25
Q

What is a stage 3 granuloma?

A

From weeks to 1 month
The central area can caseate or become dense with macrophages and mineralize
Lymphocytes, plasma cells, a zone of fibroblasts, and a fibrous connective tissue capsule surround this core

26
Q

What is a stage 4 granuloma?

A

From several weeks to months
The lesion can be walled off by a dense capsule
Regions within the lesion can become mineralized and overtake the surrounding tissue

27
Q

What is a good example of diffuse granulomatous inflammation?

A

Johne’s in cattle

28
Q

How can you identify that there is diffuse granulomatous inflammation?

A

There are no well defined modules

There is a diffuse accumulation of epithelioid macrophages

29
Q

What is lymphocytic inflammation?

A

Accumulation of lymphocytes

30
Q

What is seen grossly with lymphocytic inflammation?

A

Difficult to determine grossly

If infiltrates are extensive, the tissue may have a tan/white color

31
Q

What is seen microscopically with lymphocytic inflammation?

A

Lymphocytes present

Can be mixed with plasma cells

32
Q

What are causes of lymphocytic inflammation?

A

Certain viral infections (rabies, WNV, EEE
Certain bacterial infections (listeria)
Some parasitic infections (Toxoplasma gondii)

33
Q

What are effects of lymphocytic inflammation?

A

Indicates the immune response is occurring against an agent

Many cases involving the nervous system are fatal

34
Q

Describe lymphocytes

A

Small cells, with very little cytoplasm
Lymphocytes entered unresolved areas of acute inflammation within 24-48 hours
In some organs (brain), will have a perivascular pattern

35
Q

What are B cells?

A
  1. Lymphocytes take up and present antigen

2. Differentiate into plasma cells- secrete immunoglobulins

36
Q

When do plasma cells predominate?

A

Certain chronic inflammatory conditions

37
Q

Describe eosinophilic granulomas

A

Recruited into and stimulated to proliferate- IL-5 and eotaxin
Dense infiltrate of eosinophils with macrophages, varying numbers of lymphocytes and plasma cells

38
Q

What does fibrosis stimulate?

A

Fibroblasts

39
Q

What do fibroblasts contribute to?

A

Structural integrity of tissue

40
Q

What are fibroblasts responsible for?

A

Synthesis of collagen and extracellular matrix proteins

Produce cytokines and chemokines that regulate the extracellular environment

41
Q

What do fibroblastic growth factors signal?

A

Proliferation

42
Q

What is fibrous connective tissue?

A

Dense accumulation of fibroblasts and collagen

With time, connective tissue becomes more dense and fewer inflammatory cells

43
Q

What are the 4 phases of wound healing?

A

Hemostasis
Inflammation
Proliferation
Remodeling

44
Q

What is the hemostasis phase of wound healing?

A

Platelet plug, angiogenesis

45
Q

What is the inflammation phase of wound healing?

A

Cardinal signs of inflammation

Clean up cell debris from tissue injury

46
Q

How does excessive inflammation effect wound healing?

A

It inhibits it

47
Q

What is the proliferation phase of wound healing?

A

New endothelium, epithelium, and connective tissue to restore normal function

48
Q

What is the remodeling phase of wound healing?

A

Remodeling of granulation tissue and conversion to mature connective tissue

49
Q

What does wound repair require?

A

Extracellular matrix and it must be resynthesized

50
Q

What is granulation tissue?

A

Fibroblasts and endothelial cells proliferate to fill in tissue defects

51
Q

How do fibroblasts grow?

A

Parallel to the wound surface and perpendicular to the proliferating capillaries

52
Q

What can excessive granulation tissue lead to?

A

A hypertrophic scar

53
Q

How is healing affected if the basement membranes are damaged?

A

Healing will take longer

54
Q

What happens if healing is delayed?

A

Altered healing can occur leading to extensive fibrosis

55
Q

What is 1st intention healing?

A

Primary intention healing
When edges are directly apposed
Heals rapidly with little trace of wound

56
Q

What is 2nd intention healing?

A

Gaping wound or infected wound

Connective tissue disorganized

57
Q

What is epithelialization?

A

Epithelial cells at periphery proliferate

Very rapid in 1st intention healing

58
Q

What must epithelialization move along?

A

A basement membrane

59
Q

Describe bone healing

A

Hematoma
Fibroblast proliferation and mesenchymal proliferation
Callus formed (primary)
Secondary callus formed

60
Q

What inhibits fracture repair?

A
Malnutrition
Infection
Instability
Necrotic bone fragments
Movement at site
Inadequate blood supply