Acute and Chronic Inflammation Flashcards

1
Q

State the 5 cardinal signs of inflammation.

A
Swelling
Redness
Heat
Pain
Loss of function
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2
Q

Identify types of stimuli that lead to inflammation. (5)

A
Infectious agents
Toxins
Necrotic tissue
Foreign bodies
Autoimmunity
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3
Q

Name the major differences between acute and chronic inflammation. (5 categories)

A

Acute:

  • Rapid onset
  • Short duration
  • Exudative edema
  • Neutrophils and macrophages
  • Non-specific immune response

Chronic:

  • Insidious onset
  • Long duration
  • Fibrosis, vascular proliferation, and tissue destruction
  • Lymphocytes, macrophages, plasma cells
  • Immunospecific
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4
Q

Identify the stages in endothelial adhesion and transmigration.

A

Called DIAPEDESIS

  1. Margination: leukocyte redistribution to enable adhesion
    - -Vascular changes produce slower flow (stasis) -> leukocytes become more peripheral
  2. Rolling: selectins and ligands; low affinity with fast off rate, easily disrupted by blood flow
  3. Adhesion: activated integrins bind immunoglobulin family strongly
  4. Transmigration: WBCs secrete collagenases to pierce basement membrane
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5
Q

Name the four general families of adhesion molecules and give specific examples of each.

A
  1. Selectins:
    - -P-selectin (platelets)
    - -E-selectin (endothelium)
    - -L-selectin (leukocytes)
  2. Glycoproteins:
    - -PSGL-1
    - -ESL-1
    - -CD34
    - -Glycam 1
  3. Immunoglobulins
    - -ICAM-1 (intercellular)
    - -VCAM-1 (vascular)
    - -PECAM-1 (platelet-endothelial)
  4. Integrins (on leukocytes)
    - -LFA-1, MAC-1
    - -VLA-4
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6
Q

Identify which adhesion molecule family is generally complimentary to members of which other family.

A

Selectins bind glycoproteins

Integrins (on leukocytes) bind Ig family (on endothelium)

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7
Q

Name the endogenous and exogenous chemoattractants important in neutrophil chemotaxis. (3 endogenous, 1 exogenous)

A

Endogenous:

  • Cytokines (IL-8)
  • Complement (C5a)
  • Arachidonic acid metabolites (LTB4)

Exogenous:
-N-formyl-methionine

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8
Q

Explain the neutrophilic mechanism for killing and degradation of bacteria.

A

Respiratory burst: coupling of phagocytosis with rapid oxidative reaction to generate ROS within the lysosome
—-Uses phagocyte oxidase in lysosomal membrane -> superoxide -> H2O2

H2O2-MPO-halide system: converts H2O2 -> bleach

Inducible NO synthase -> NO -> OONO (peroxynitrite, highly ROS)

Also have substances in granules (lysozyme, elastase, etc.)

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9
Q

Identify categories of disease caused by inappropriate activation of the inflammatory response.

A

Autoimmunity: inappropriate defense reaction against host tissue

Allergy: excessive defense reaction against harmless environmental agents

Toxic agents: prolonged exposure to non-degradable exogenous material/endogenous toxic agents -> damage

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10
Q

Name three causes of chronic inflammation.

A
  1. Persistent infections: DTH against difficult to eradicate pathogens, especially TB
  2. Immune-mediated inflammatory disease
    - Autoimmunity
    - Allergy
  3. Prolonged exposure to toxic agents
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11
Q

Identify the characteristic cell types found in acute and chronic inflammation.

A

Acute:

  • NEUTROPHILS
  • Eosinophils (if allergy, parasites)
  • Lymphocytes (if viral)
  • Monocytes/macrophages

Chronic:

  • MACROPHAGES
  • T cells: CD4 -> macrophages, CD8 -> viral infections
  • B cells
  • Plasma cells
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12
Q

Describe the pathogenesis of granulomatous inflammation.

A

A collection of macrophages
Often appear epitheliod (open nucleus, lots of cytoplasm) or have fused “giant cells” with peripheral or random nuclei
Often surrounded by a “collar” of lymphocytes and plasma cells (in infectious types)

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13
Q

Name and define the four morphologic patters of acute inflammation.

A

Serous: thin, watery fluid from plasma or mesothelial cell secretion (as in skin blister [vesicle or bulla])

Fibrinous: increased vascular permeability allows larger molecules (fibrinogen) -> extravascular space -> fibrin deposits

Purulent (suppurative): composed of neutrophils, liquefactive necrosis, and edema

Ulcer: local defect of the surface of an organ or tissue produced by sloughing of inflamed and necrotic tissue

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14
Q

Define inflammation.

A

A coordinated and complex host response to a stimulus involving soluble mediators, vascular reaction, and cellular and humoral elements resulting in the movement of fluid and leukocytes from the blood to extravascular tissues

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15
Q

Define acute inflammation. List its three major components.

A

Rapid host response that serves to deliver leukocytes and plasma proteins (antibodies) to sites of infection or tissue injury

Major components: vasodilation, increased vascular permeability (most commonly from retraction of endothelial cells), emigration and activation of leukocytes to focus of injury

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16
Q

List the four types or receptors used to recognize microbes and dead tissue. Briefly state what each recognizes.

A
  1. Toll-like receptors: bacterial products (LPS), viral products (dsRNA)
  2. GPCRs: bacterial peptides (N-formylmethionyl residues), chemokines (C5a), lipid mediators
  3. Opsonin receptors: IgG, C3b, mannose-binding lectin
  4. Cytokine receptors: IFNgamma
17
Q

How is an inflammatory response terminated?

A

Passive: neutrophils die and are degraded

Active:

  • Switch from leukotrienes to lipoxins
  • Macrophages -> anti-inflammatory cytokines (TGF-beta, IL-10)
  • Anti-inflammatory mediators (resolvins, protectins)
  • IL-13, IL-4
18
Q

Define chronic inflammation. List its four main characteristics.

A

Inflammation of prolonged duration in which inflammation, tissue injury, and attempts at repair coexist in varying combination

  • Mononuclear cell infiltrate (NO NEUTROPHILS; lymphocytes, plasma cells, macrophages)
  • Tissue destruction
  • Angiogenesis
  • Fibrosis
19
Q

Define scar. Why is scar formation bad? (3 reasons)

A

Replacement of nonregenerated parenchymal cells with connective tissue

Bad because:

  1. Has no function
  2. Can obstruct, block, or constrict normal tissue, thus diminishing or destroying their function
  3. Can bind together structures/tissues that should remain independent
20
Q

Define adhesion.

A

When scar tissue binds tissue together

21
Q

Define abscess.

A

Localized collections of suppurative (purulent) inflammation
–Neutrophils, liquefactive necrosis, edema fluid

Center = necrotic leukocytes and tissue cells
First ring = preserved neutrophils
Outer ring = vascular dilation, fibroblastic proliferation

22
Q

Discuss changes seen in acute appendicitis. (2)

A
  • -Extensive neutrophil infiltration

- -Ulceration of mucosa

23
Q

Discuss changes seen in acute pyelonephritis of the kidney. (1) What causes this?

A

–Many neutrophils in interstitium

Cause: bacteria ascending the urinary tract

24
Q

Define empyema.

A

Usually caused by an infection that spreads from the lung

Leads to a buildup of pus in the pleural space

25
Q

Discuss changes seen in acute pleuritis with empyema in the lung. (6)

A
  • -Bacterial colonies
  • -Clumps of neutrophils in various stages of disintegration
  • -Fibrin deposition, especially in pleural space
  • -Granulation tissue: lots of capillaries and immature fibroblasts
  • -Bronchiolitis: lots of neutrophils in bronchi
  • -Pneumonia: alveolar parenchyma infiltrated with neutrophils
26
Q

Discuss changes seen in bacterial pneumonia of the lung. (5)

A
  • -Alveoli filled with neutrophils
  • -Pale pink homogenous edematous fluoid present in alveoli
  • -Scattered fibrin deposition
  • -Red cells in alveoli (generally lysed)
  • -Alveolar macrophages present