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Pathology Exam 1 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the goals of inflammation?

A
  1. Eliminate initial cause of cell injury
  2. Remove necrotic cells/tissue
  3. Initiate process of repair
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2
Q

What are 2 components of the inflam process?

A

WBCs and plasma proteins

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3
Q

What is inflammation induced by?

A

Chemical mediators produced by damaged host cells (i.e. cytokines)

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4
Q

T or F: Inflamm is normally controlled and self-limited

A

True

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5
Q

What does inappropriate inflamm response when there are no foreign substances to fight off lead to?

A

Autoimmunity

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6
Q

What are the 5 cardinal signs of inflamm?

A
  1. Heat (calor)
  2. Redness (rubor)
  3. Swelling (tumor)
  4. Pain (dolor)
  5. Loss of function
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7
Q

What cells are involved in inflamm?

A
  1. Platelets
  2. Granulocytes (PMNs, Mast)
  3. Monocyte/Macrophages
  4. Lymphocytes
  5. Fibroblasts
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8
Q

What proteins are involved in inflamm?

A
  1. Complement
  2. Pentraxins
  3. MBL
  4. Ficolins
  5. Coagulation
  6. Kininogens
  7. Proteoglycans
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9
Q

What are granulocytes?

A

Phagocytes (PMN - polymorphonucleaur leukocytes)

  • Basophil
  • Eosinophil
  • Neutrophil
  • Mast cells
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10
Q

What are monocytes?

A
  • Longer-lived phagocytes
  • Present pieces of pathogens to T cells -> recognized in future and killed
  • Leave bloodstream -> macrophages (which remove dead cell debris and attack microbes)
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11
Q

What are lymphocytes?

A

Produce cytokines, bind antigens of infected/tumor cells and kill them

  • B cells
  • T cells
  • NK cells
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12
Q

What are mast cells?

A
  • Contains granules full of histamine
  • Most commonly known for role in allergy
  • Involved in defense of pathogens
  • Live in tissue
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13
Q

What comprises the cellular infiltrate in acute inflamm vs. chronic?

A

Acute = mainly neutrophils

Chronic = monocytes/macrophages/lymphocytets

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14
Q

What can trigger an acute inflamm rxn?

A
  1. Infections (bacterial, viral, fungal, parasitic) and microbial toxins
  2. Tissue necrosis: ischemia, trauma, physical/chemical injury (thermal injury, irradiation, some envir chemicals)
  3. Foreign bodies (splinters, dirt, sutures)
  4. Immune rxns (aka hypersensitivity rxns)
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15
Q

What are the 2 major components of acute inflamm?

A
  1. Vascular changes
  2. Cellular events
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16
Q

What vascular changes occur in acute inflamm?

A
  1. Vasodilation
  2. Vascular permeability
  3. Increased adhesion of WBCs
17
Q

What cellular events occur in acute inflamm?

A

Cellular recruitment and activation of NEUTROPHILS

18
Q

What causes vasodilation in acute inflamm? What results from vasodilation?

A
  • NO, histamine -> vascular smooth muscle vasodilation
  • Decreases BP; Increases blood flow -> heat/redness
  • Microvasculature becomes more permeable -> protein-rich fluid into extravascular tissues -> RBCs in flowing blood more concentrated -> stasis (hyperviscosity, slows blood flow)
  • Margination of circulating leukocytes and endothelial activation
19
Q

What causes changes in vessel permeability in acute inflamm?

A

Histamines, bradykinins, leukotrienes cause endothelial cell contraction that widens intercellular gaps of venules

20
Q

What forms as a result of increased permeability of the vasculature in acute inflamm?

A

An early transudate (protein-poor filtrate of plasma) gives way to exudate (protein-rich filtrate) into extracellular tissues, which leads to:

  • Reduction of intravascular osmotic pressure
  • Increase in extravascular/interstitial osmotic pressure
  • EDEMA (water + ions)
21
Q

Why is an exudate formed instead of a transudate in acute inflamm?

A

Vascular permeability increases as a result of increase in interendothelial spaces

-Transudates are interstitial fluid accumulations caused by increased hydrostatic pressure (usually b/c of reduced venous return)

22
Q

Through what sequence of events do leukocytes leave the vasculature in acute inflamm?

A
  1. Margination and rolling
  2. Activation and adhesion
  3. Transmigration
23
Q

What happens in “margination and rolling” during acute inflamm?

A
  • Fluid (exudate) leaves the vessel -> leukocytes “marginate” along endothelial surface
  • In the process of “rolling” inidividual and then rows of leukocytes tumble slowly along the endothelium, adhere through surface adhesion molecules on endothelial cells and their complementary ligands on leukocytes
24
Q

What is “adhesion” in acute inflam mediated by?

A

Selectin family (adhesion molecules)

  • E-selectin (endothelium)
  • P-selectin (platelets, endothelium)
  • L-selectin (leukocytes)
25
Q

What happens during “activation and adhesion” in acute inflamm?

A

Selectins that are upregulated on endothelium by cytokines (TNF-alpha, IL-1) at injury sites bind leukocyte surface molecules, i.e. Sialyl-Lewis X modified GP, P-selectin glycoprotein ligand (PSGL-1), integrins, and CD34

26
Q

When does transmigration (diapedesis) in acute inflamm occur?

A

After firm adhesion within the system of venules and capillaries via PECAM-1 (CD31) (platelet-endothelial cell adhesion molecule) on endothelial cells, neutrophils, monocytes/macrophages, lymphocytes

27
Q

During transmigration during acute inflamm, what does upregulation of endothelial cell ligands (integrins) for adhesion molecules result in?

A

Activation/adhesion of different populations of leukocytes (monocytes, lymphocytes, etc)

28
Q

What is the source and action of histamine?

A
  • Source: mast cells, basophils, platelets
  • Action: vasodilation, increased vascular permeability, endothelial activation
29
Q

What is the source/action of prostaglandins?

A
  • Source: Mast cells, leukocytes
  • Action: Vasodilation, pain, fever
30
Q

What is the source/action of leukotrienes?

A
  • Source: Mast cells, leukocytes
  • Action: Increased vascular permeability, chemotaxis, leukocyte adhesion/activation
31
Q

What is the source/action of cytokines (TNF, IL-1, IL-6)?

A
  • Source: Macrophages, endothelial cells, mast cells
  • Action:
    • Local = endothelial activation (expression of adhesion molecules)
    • Systemic = fever, metabolic abnormalities, hypotension (shock)
32
Q

What is the source/action of chemokines?

A
  • Source: Leukocytes, activated macrophages
  • Action: Chemotaxis, leukocyte activation
33
Q

What is the source/action of platelet-activating factor?

A
  • Source: Leukocytes, mast cells
  • Action: Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst
34
Q

What is the source/action of complement?

A
  • Source: Plasma (produced in liver)
  • Action: Leukocyte chemotaxis/activation, direct target killing (membrane attack complex), vasodilation (mast cell stimulation)
35
Q

What is the source/action of kinins?

A
  • Source: Plasma (produced in liver)
  • Action: Increased vascular permeability, smooth muscle contraction, vasodilation, pain

Pathology Exam 1 (5 decks)

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