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Cell Biology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

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1
Q

What is inflammation?

  • definition?
  • specific or not?
  • what cells/materials are involved?
  • what can it lead to?
A

Inflammation is a vascularized protective response to damage or microorganisms

  • non-specific, universal
  • blood vessels (endothelium), leukocytes, and chemical mediators (innate immune system)
  • can lead to adaptive immune response
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2
Q

Acute vs. Adaptive Immune system?

A

Acute:

  • rapid onset
  • short duration
  • characterized by fluid extravasation
  • cells: neutrophils

Adaptive:

  • slow onset
  • long duration
  • characterized by fibrosis
  • cells: macrophages and lymphocytes
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3
Q

What are the 5 cardinal signs of inflammation?

A 
Rubor (redness)
Tumor (swelling)
Dolor (pain)
Calor (heat)
Functio Laesa (loss of function)
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4
Q

Acute Inflammation:

The acute inflammatory pathway can be divided into three main components:

A
  1. Vasodilation and vascular permeability
  2. Leukocyte reaction
  3. Chemical mediators
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5
Q

Vascular changes in acute inflammation

  • -> list 2 (and their causes)
  • -> what cardinal signs do they cause
  • -> what do they do to blood flow
A

Changes:
1. vasodilation (from histamine, NO, and PGDs)
- leads to rubor and calor
2. vascular permeability (from histamine, C3a, C5a, and leukotrienes)
- leads to tumor
These vascular changes lead to blood stasis

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6
Q

Blood vessel pressures

A
  1. Hydrostatic pressure
    - the pressure of the fluid inside blood vessels on the endothelium
    - there is higher hydrostatic pressure at the arteriolar ends of capillaries, allowing oxygen and other nutrients to leave the blood vessel and get to the tissues; at the venular ends of capillaries, hydrostatic pressure is lower (all nutrients have left).
    Net OUTFLOW
  2. Osmotic pressure
    - the pressure of outside fluid into the blood vessels, created by the osmotic pulls because of the cells and plasma inside the blood vessels
    - lower at the arteriolar ends of the capillaries, higher at the venular ends of the capillaries (when fluid has exited the capillaries). This allows for nutrients and waste products to enter the capillaries.
    Net INFLOW

Normally, net inflow = net outflow

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7
Q

Fluid leakage inflammatory vs. non-inflammatory

A

Inflammatory:
Exudate - fluid has higher concentration of cells and proteins (and higher specific gravity)
- occurs with inflammation (permeability) and damage

Transudate - fluid has lower concentration of cells and proteins and low specific gravity
- occurs with increase in hydrostatic pressure or decrease in osmotic pressure (net mvm’t out)

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8
Q

Mechanisms of increased vascular permeability (2)

A
  1. Inflammatory mediators
    - histamine and other mediators
    - causes endothelial cells to retract, making spaces between the cells to allow proteins and cells to escape
    - rapid, controlled response
  2. Damage
    - damage to the endothelial cells also results in spaces between the cells, allowing material to leave the cell
    - may be long-lived, not controlled
    - e.g. burns, toxins
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9
Q

What happens when fluid accumulates in pleural cavity?

  • name
  • treatment
  • how do we know what the cause of the accumulation is? provide examples of the causes.
A
  • Pleural effusion
  • Treat through thoracocentesis
  • If you test the fluid, you can determine if it is an exudate or a transudate. Exudate = inflammation. Transudate = not inflammation.
  • Exudate example: acute pneumonia
  • Transudate example: congestive heart failure (heart cannot pump properly, there is a back up of fluid, increased hydrostatic pressure in alveolar capillaries, leading to transudate pleural effusion)
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10
Q

Acute Inflammation:

  • What is first leukocyte
  • List functions (3)
A
  • Neutrophils
  • 3-fold:
    1. Phagocytose aggravators
    2. Kill microorganisms
    3. Degradation and removal of necrotic tissue
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11
Q

List steps of leukocytic response (3)

A
  1. Neutrophil extravasation
  2. Chemotaxis
  3. Phagocytosis
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12
Q

Neutrophil Extravasation

- list steps

A
  1. Margination: neutrophils in blood vessels have receptors, and begin attaching to receptors on the endothelial lining called selectins. These are transient attachments and help slow down the neutrophil
  2. Neutrophils roll along the endothelial wall while attaching to these receptors
  3. Adhesion: neutrophils attach to integrins, which are receptors on the endothelium. These attachments are stronger, and the neutrophil stops.
  4. Diapedesis: mediators work to help the neutrophil slip through the permeable endothelium
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13
Q

Chemotaxis

A

Once neutrophils leave the blood vessels, they must know where to go to aid in the inflammatory process.

They “sniff” to find the areas that are most affected, by sensing the concentration of chemical stimulus and moving toward areas with the highest concentration of chemoattractants (including bacterial products and chemical mediators)

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14
Q

Phagocytosis

A

1) neutrophils must recognize offending agents. Does this by recognizing opsonin, which are markers that attach to the offending agent
2) Engulf: forms phagolysosome.
3) Degrade (by ROS or enzymes):
- fusion of phagolysosome with cell lysosome (containing enzymes and ROS) results in degradation
- ROS: there are enzymes that create ROS in the phagolysosome.

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15
Q

What’s the problem with inflammation? So how does inflammation need to be handled by the body?

A
  • the degrading enzymes and ROS are just as harmful to normal tissues as they are to offending agents
  • inflammation must be tightly controlled and regulated
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16
Q

Chemical Mediators

- List/organize (2 types: 1st one has 2 subtypes)

A

Cellular Chemical Mediators:
1) Preformed Mediators
- vasoactive amines (histamine, serotonin)
- lysosomal enzymes in leukocytes (proteases, etc)
2) Produced de novo
- Arachidonic Acid derivatives (thromboxanes, prostaglandins, leukotrienes)
- Nitric Oxide
- Cytokines (tumour necrosis factor, interleukin-1)
Plasma protein-derived chemical mediators

17
Q

Preformed vs. Produced de novo?

Both?

A

preformed:

  • rapid release –> rapid onset of action
  • stored in granules

de novo:
- slow release (must first be made) –> slow onset of action

In both:

  • short-lived
  • extensive cross-talk and cross-activation
18
Q

Histamine:

  • where is it stored?
  • what triggers degranulation?
  • what are its effects?
A
  • in granules in basophils or mast cells
  • triggers: extreme temperatures, exposure to allergens, C5a and C3a
  • effects: vasodilation, endothelial cell contraction (vascular permeability), runny nose and bronchial constriction
19
Q

Arachidonic Acid metabolites:

  • where do they come from?
  • what stimulates their release?
A
  • from fatty acids (phospholipids) in plasma cell membrane of damaged cells or leukocytes
  • cell damage or C5a
20
Q 
TNF/IL-1 Pathway
- what is it activated by?
- effects:
Local effects (3) and their end result (2)
Systemic effects (3) and end result (1)
A

Activated by macrophages and other cells, which are themselves activated by cytokines, microbial agents, and toxins.

Local effects:
1) Vascular endothelium
- increased expression of leukocyte adhesion molecules
- production of IL-1, chemokines
- increase pro-coagulation; decrease anticoagulation activity
2) Leukocytes
- Activation of leukocytes 
- production of cytokines
1+2 response = inflammation
3) Fibroblasts
- proliferation of fibroblasts
- production of collagen
3 response = repair

Systemic effects:

  • fever
  • leukocytosis
  • decreased appetite
  • increase fatigue
  • increase acute-phase proteins

response: systematic response to inflammation

21
Q

What is the link between the inflammatory and coagulation pathways?

A

Thromboxane

  • -> produced by arachidonic acid, which is created by immune cells or damaged cell membranes (inflammatory side)
  • -> thromboxane acts to coagulate blood (vasoconstriction and platelet aggregation)

Inflammation can lead to coagulation

22
Q

Arachidonic Acid pathway:

  • what types of effects are there? why? (general)
  • List 2 pathways
  • -> specific products and their effects
  • -> any inhibitors
A

Effects: many, some contradictory (to keep things in check; tightly regulate)
1) 5-lipooxygenase –> Leukotrienes
effects: vascular permeability and chemotaxis; also inhibition of neutrophil adhesion and inhibition of chemotaxis
2) Cyclooxygenase –> Prostaglandins and Thromboxane
PGDs: vasodilation and increased vascular permeability
Thromboxane A2: platelet aggregation, vasoconstriction
- cyclooxygenase is inhibited by Cox1 and Cox2 inhibitors, like aspirin and indomethacin (aspirin is anti-inflammatory medication)

23
Q

Plasma protein derived mediators of inflammation

  • list 2 types of mediators
  • what pathways/processes are each involved in?
A

1) Complement
- family of proteins (C1-C9); innate and adaptive immune system
- circulate in inactive form in blood
- activated by microbes (alternate) or immunoglobin (classical)
- goal is activation of C3 and C5
2) Coagulation and Kinin systems
- activation of kinin cascade and intrinsic clotting pathway
- Factor XII (Hageman factor)

24
Q

Complement system:

  • goal?
  • cleavage process
  • What does each important complement do?
A
  • activation of C3 and C5
  • once C3= C3a and C3b; C3b helps with cleavage of C5
  • C3a and C5a are anaphylatoxins - help release histamine, which leads to vasodilation and permeability
  • C5a also is a chemotactic agent to recruit neutrophils
  • C5a also helps release of AA derivatives
  • C3b is an opsonin (tags offending agents for identification before phagocytosis)
  • C5b is part of MAC (membrane attack complex), which directly kills microbes
25
Q

Coagulation and Kinin systems

  • what factor?
  • what does it activate?
  • products of pathways (3) and what they do
A
  • Hageman factor (XII)
  • Kinin cascade; intrinsic clotting pathway
    1) Bradykinin
  • produced by Kinin cascade
  • responsible for dolor (pain)
    2) Thrombin
  • produced by coagulation pathway
  • can activate arachidonic acid via the cyclo-oxygenase pathway
    3) Plasmin
  • enzyme from clotting pathway (breaks down clots)
  • can activate complement proteins
26
Q

Chemical Mediators in Inflammation

  1. Vasodilation
  2. Vascular Permeability
  3. Chemotaxis and Activation
  4. Opsonization
  5. Fever
  6. Pain
  7. Tissue Damage
A
  1. Vasodilation (Prostaglandins, Nitric oxide, Histamine)
  2. Vascular Permeability (Histamine, Leukotrienes, C3a, C5a)
  3. Chemotaxis and Activation (C3a, C5a, TNF, IL‐1,
    Leukotriene B4)
  4. Opsonization (C3b)
  5. Fever (TNF, IL‐1)
  6. Pain (Bradykinin, some prostaglandins)
  7. Tissue Damage (lysosomal enzyme, reactive oxygen
    species, nitric oxide)
27
Q

Morphologic hallmarks of inflammation (3)

Morphologic patterns of acute inflammation (3)

What does the pattern depend on?

A 
Hallmarks:
- vasodilation
- vessels engorged with blood
- exudation of fluid and leukocytes
Patterns:
- Serous
- Fibrinous
- Suppurative/purulent (pus)
Depend on?
- site of injury
- nature of injury
- severity of injury
28
Q

Describe each pattern of inflammation:

1) Serous
2) Fibrinous
3) Suppurative

A

1) Serous
- mild injury (mild burn; viral infection)
- minimal vascular permeability
- fluid&raquo_space;> leukocytes
2) Fibrinous
- marked vascular permeability
- local procoagulant stimulus (lots of clotting)
- typical of body cavities (pleura, pericardium)
3) Suppurative
- collection of neutrophils (pus)
- leukocytes&raquo_space;> fluid
- often related to microbial organisms

29
Q

Outcomes of acute inflammation (3)

A

1) complete resolution
- limited injury/little tissue destruction
- all cells replaced, function returns to normal
2) healing by connective tissue replacement (Fibrosis/scarring)
- when there is extensive injury or tissues are incapable of regenerating themselves
- connective tissue grows into area of damage, forming a scar
3) Progression to chronic inflammation

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