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Pathology > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

Characteristics of chronic inflammation

A
  • predominance of mononuclear cells (macrophages, lymphocytes, plasma cells)
  • vascular changes are minimal
  • increased CT (fibrosis)
  • alteration in tissue architecture
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2
Q

Why does chronic inflammation occur?

A
  • neutrophils are short lived and they signal macrophages –> macrophages are longer lived and proliferate in tissues
  • persistence of antigen
  • some stimuli signal chronic inflammatory cells directly
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3
Q

_____ occurs because acute inflammation fails to eliminate stimulus

A

Abscesses

  • liquefaction due to neutrophil enzymes
  • color of exudate depends on pigment produced by inciting stimulus
  • fibroblasts produce collagen and form thin CT around exudate –> matures into a fibrous capsule (takes a week to form a wall
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4
Q

Microabscesses

A

Seen histologically, do not have a true capsule, is just an accumulation of neutrophils

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5
Q

The inner wall of an abscess is _____

A

Granulation tissue

  • pyogenic membrane with increased collagen
  • full of vessels that allow continual recruitment of neutrophils
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6
Q

NAG

A

Neoplasia, abscess, granuloma

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7
Q

Classically activated macrophage

A
  • microbicidal actions
  • phagocytosis
  • inflammation
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8
Q

Alternatively activated macrophage

A
  • anti-inflammatory effects

- wound repair, fibrosis

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9
Q

Granulomatous means ________

A

MACROPHAGES!

- dependent upon presence of indigestible organisms/particles or presence of cell mediated immunity to inciting agent

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10
Q

Gross appearance of granulomatous inflammation

A
  • diffusely thickened tissue

- firm nodules of various sizes

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11
Q

Micro appearance of granulomatous inflammation

A
  • numerous macrophages present

- accompanied by variable numbers of lymphocytes and plasma cells, and CT

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12
Q

Effect of granulomatous inflammation

A
  • chronic infection which the body cannot eliminate

- interfere with organ function

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13
Q

What are 4 causes of granulomatous inflammation?

A
  • bacteria (resistant to phagocytosis): mycobacteria, actinobacilli, archanobacterium
  • fungi: hisoplasma, cryptococcus, blastomyces
  • parasitic diseases: parasitic larvae that die during migration
  • foreign bodies: wood, grass awns, suture material
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14
Q

Eqithelioid macrophages

A

Abundant eosinophilic cytoplasm and large pale nuclei

- more secretory and less phagocytic than typical macrophages

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15
Q

Giant cells

A

Large multinucleated cells

- arise from fusion of macrophages

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16
Q

When macrophages are in aggregates they are referred to as ________

A

Granulomas

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17
Q

Classic granulomas

A
  • central core of caseous necrosis
  • zone of epithelioid macrophages and giant cells
  • zone of lymphocytes (predominantly T cells)
  • outer layer of fibroblasts and fibrosis
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18
Q

Diffuse vs nodular

A

Morphologic forms based on immunologic response

  • TH2: diffuse granulomatous inflammation
  • TH1: nodular granulomas
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19
Q

TH1

A
  • cell mediated immunity and inflammation
  • intracellular pathogens
  • autoimmunity
  • inflammation
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20
Q

TH2

A
  • antibody mediated immunity
  • extracellular parasites
  • asthma, allergy
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21
Q

Stage 1 granuloma

A

Days after infection

  • lesion site is infiltrated by neutrophils, monocytes, macrophages, and lymphocytes
  • epithelioid macrophages form
22
Q

Stage 2 granuloma

A

From 48 hrs to multiple days and weeks
- lesions contain macrophages, epithelioid macrophages, thin rims of fibrous CT, variable numbers of lymphocytes and MCGs can form

23
Q

Stage 3 granuloma

A

From weeks to 1 month

  • central area can caseate or become dense with macrophages and mineralize
  • lymphocytes, plasma cells, a zone of fibroblasts, and a fibrous CT capsule surround this core
24
Q

Stage 4 granuloma

A

From several weeks to months

  • lesion can be walled off by a dense capsule
  • regions within the lesion can become mineralized and overtake the surrounding tissue
25
Q

Rhodococcus equi

A

Pneumonia in foals due to failure of phagolysosomal fusion

  • decreased IFN-gamma which is a key signal for macrophage activation
  • granulomatous to pyogranulomatous pneumonia
26
Q

Diffuse granulomatous inflammation

A

No well defined nodules, diffuse accumulation of epithelioid macrophages
- ex: Johne’s disease in cattle due to M. paratuberculosis

27
Q

Gross appearance of lymphocytic inflammation

A

Difficult to determine, if infiltrates are extensive, tissue may have a tan/white color

28
Q

Micro appearance of lymphocytic inflammation

A

Lymphocytes present, can be mixed with plasma cells

29
Q

Causes of lymphocytic inflammation

A
  • viral infection (esp. viruses that infect the brain)
  • bacterial infection (listeria)
  • parasitic infection (t. gondii)
30
Q

Effects of lymphocytic inflammation

A

Indicates immune response is occurring against an agent

- cases involving nervous system are fatal

31
Q

Lymphocytes

A

Small cells, with very little cytoplasm

  • lymphocytes enter area of unresolved acute inflammation within 24-48 hrs
  • some organs (brain) have a perivascular pattern
32
Q

B cells

A
  • lymphocytes take up and present antigen

- differentiate into plasma cells, secrete immunoglobulins

33
Q

Eosinophilic granulomas

A

Recruited into and stimulated to proliferate (IL-5, eotaxin)

- dense infiltrate of eosinophils with macrophages, varying numbers of lymphocytes and plasma cells

34
Q

Fibroblasts

A

Contribute to structural integrity of tissue

  • synthesis of collagen and ECM proteins
  • produce cytokines and chemokines that regulate extracellular environment
  • fibroblastic growth factors signal proliferation, continued release of factor can lead to extensive fibrosis
35
Q

Fibrous CT

A

Dense accumulation of fibroblasts and collagen

- with time, CT becomes more dense and fewer inflammatory cells

36
Q

Is fibrosis cellular?

A

NO

37
Q

What are the 4 phases of wound healing?

A
  • hemostasis
  • inflammation
  • proliferation
  • remodeling
38
Q

Hemostasis

A

Platelet plug, angiogenesis

39
Q

Inflammation

A

Cardinal signs of inflammation, clean up cell debris from tissue injury
- excessive inflammation inhibits wound healing

40
Q

Proliferation

A

New endothelium, epithelium and CT to restore normal function

41
Q

Remodeling

A

Remodeling of granulation tissue and conversion to mature CT

42
Q

Wound repair requires ______

A

ECM and must be resynthesized

43
Q

______ and _____ proliferate to fill in tissue defects

A

Fibroblasts and endothelial cells

- fibroblasts grow parallel to wound surface and are perpendicular to proliferating capillaries

44
Q

Proud flesh

A

Excessive granulation tissue that leads to a hypertrophic scar

  • skin wounds of distal limbs of horses
  • looks granular on surface and often bleeds
45
Q

T/F: granulation tissue is the same as granulamatous inflammation

A

FALSE!!

46
Q

Repair

A

If BM is damaged, healing will take longer

  • if healing is delayed, altered healing occurs = extensive fibrosis
  • -> inflammation, large tissue defect with loss of BM
47
Q

1st intention

A

Primary intention healing

  • when edges are directly apposed (surgery)
  • heals rapidly with little tract of wound
48
Q

2nd intention

A

Gaping wound or infected wound

- CT disorganized

49
Q

Epithelialization

A

Epithelial cells at periphery proliferate

  • very rapid in 1st intention healing
  • must move along BM
  • -> without a BM cells do not have a clear path, remaining cells will spread out to cover defect until cells can divide and replace
50
Q

Bone healing

A

Hematoma –> fibroblast and mesenchymal proliferation, osteoblasts for bone is immature –> callus formed (primary) and will see cartilage –> secondary callus formed (stronger lamellar bone)

51
Q

Inhibition of bone repair

A
  • malnutrition
  • infection
  • instability
  • necrotic bone fragments
  • movement at site
  • inadequate blood supply

Pathology (19 decks)

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