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IDIT Exam 3 - Pathology > Inflammation-Mesa > Flashcards

Inflammation-Mesa Flashcards

1
Q

What cells are most involved in acute inflammation?

A

Neutrophils

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2
Q

What is exudate?

A
  • Leakage of proteinaceous fluid

* High specific gravity

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3
Q

What is transudate?

A
  • Acellular leakage of fluid close to water

* Low specific gravity

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4
Q

Extravasation of PMNs

A
  • Margination - neutrophils go toward walls
  • Rolling - tumbling and heaping
  • Adhesion
  • Transmigration - leukocytes leaving circulatory system
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5
Q

What is a PMN?

A

A fancy ass Neutrophil

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6
Q

What are secretins?

A

Adhesion molecules from endothelial cells

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7
Q

What are integrins?

A

Adhesion molecules from many different cell types

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8
Q

What is chemotaxis?

A
  • PMNs go to site of injury after transmigration

* Regulated by chemokines

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9
Q

What is leukocyte activation make PMNs do?

A

• Produce eicosanoids such as:

  • Prostaglandin
  • Leukotrines
  • Lipoxins
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10
Q

What are the 9 steps of inflammation?

A
  1. Vasodilation
  2. Increased vascular permeability
  3. Leakage of exudate
  4. Margination, rolling, adhesion
  5. Transmigration
  6. Chemotaxis
  7. PMN activation
  8. Phagocytosis
  9. Termination
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11
Q

Histamine

A
  • Main mediator of inflammation
  • IgE on mast cell triggers release
  • Made in mast cells, basophils, platelets
  • Causes: vasodilation, increased vascular permeability and endothelial activation
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12
Q

Serotonin

A
  • Made in platelets
  • Evokes NO synthase which generates NO (vasodilator)
  • Causes: vasodilation and increased vascular permeability
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13
Q

Complement

A

• Final product results in lysis of membrane of bacteria

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14
Q

Kinin System

A

• Bradykinin is main component

- Causes increased permeability but results in smooth muscle contraction (painful!)

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15
Q

Clotting factors

A
  • Production of fibrin (coagulation)

* Fibrinolysis - dissolves the fibrin

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16
Q

Prostaglandins

A
  • Made in mast cells and leukocytes
  • Actions: pain, fever and clotting
  • Aspirin counteracts these
17
Q

Leukotrienes

A
  • Made in mast cells

* Causes: increased vascular permeability, chemotaxis, leukocyte adhesion and activation

18
Q

Lipoxins

A
  • Inhibit chemotaxis and cause vasodilation

* Counteract leukotrienes

19
Q

Platelet-Activating Factor (PAF)

A
  • Made in leukocytes and mast cells

* Causes: vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

20
Q

Cytokines/Chemokines

A 
Cytokines
• Proteins produced by many cells
• Usually lymphocytes and macrophages
Chemokines
• Small proteins which are attractants for PMNs
21
Q

What are the 2 most powerful regulating cytokines and what produces them?

A

TNF-α and IL-2; Macrophages

22
Q

Nitric Oxide (NO)

A
  • Potent vasodilator

* Produced from asinine by NO synthase

23
Q

Lysosomal constituents - Primary granules

A 
• Azurophilic (non-specific)
• Main components:
- Myeloperoxidase
- Lysozyme
- Acid hydrolyses
24
Q

Lysosomal constituents - Secondary granules

A 
• Specific (more mature)
• Main components:
- Lactoferrin
- Lysozyme
- Alkaline
- Phosphatase
- Collagenase
25
Q

Free radicals

A

• Produced by cells in the inflammatory process

- Very toxic to microbes

26
Q

Neuropeptides

A
  • Produced in CNS

* Not a big role in acute inflammatory process

27
Q

What is Substance P used for?

A

Mood disorders

28
Q

What is Neurokinin A?

A

Acts like neurotransmitters

29
Q

What are the 3 possibly outcomes of acute inflammation?

A
  1. Hopefully 100% resolution
  2. Sometimes scarring
  3. Chronic inflammation
30
Q

What are the morphological patterns of acute inflammation?

A
  • Serous (watery)
  • Fibrinous (hemorrhagic, rich in fibrin)
  • Suppurative (pus(sy))
  • Ulcerative
31
Q

What are some causes of chronic inflammation?

A
  • Persistence of infection
  • Prolonged exposure to insult
  • Auto-immunity
32
Q

Cellular players of chronic inflammation

A
  • Lymphocytes
  • Macrophages
  • Plasma cells
  • Eosinophils
  • Mast cells
33
Q

What is a granuloma?

A

A focus of chronic inflammation consisting of a microscopic aggregation of macrophages that are transformed into epithelial-like cells

34
Q

What are the 4 components of a granuloma?

A
  1. Fibroblasts along the outside
  2. Lymphs
  3. Histiocytes
  4. Giant cells (macrophages that fuse together)
35
Q

If there is caseating necrosis in a granuloma what does that mean?

A

Tuberculosis!

36
Q

What are some clinical manifestations of chronic inflammation?

A
  • Fevers, chills
  • C-Reactive Protein (CRP)
  • Acute phase reactants (α1-α2)
  • Erythrocyte sedimentation rate (ESR) increases
  • Leukocytes
  • Increase production of various cytokines
37
Q

Serum protein electrophoresis

A
  • Albumin is the largest peak

* α1 and α2 are elevated in acute inflammation

38
Q

What are the consequences of defective inflammation?

A
  • Results in increased susceptibility to infections

* Associated with delayed wound healing

39
Q

What are the consequences of excessive inflammation?

A
  • The basis for many types of disease
  • May cause unregulated immune response (allergies) or auto-immune disorders
  • Plays a role in arteriosclerosis, ischemic heart disease and some neurodegenerative diseases

IDIT Exam 3 - Pathology (3 decks)

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