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Pathology #1 > Overview of Inflammation #2 (1/12/16) > Flashcards

Overview of Inflammation #2 (1/12/16) Flashcards

1
Q

What changes occur in blood flow during acute inflammation?

A

Vasodilation = Increased vascular permeability

*Fluid can leak out of blood vessels causing tissue edmea

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2
Q

Vasodilation is mediated by ____, ____ and ______.

A

Nitric Oxide
PG’s
Histamine

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3
Q

What is the first cell to arrive a site of acute inflammation?

A

PMN’s (Neutrophils)

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4
Q

What are the 2 types of fluid that accumulate in inflammation?

A

Transudate = low protein fluid, low specific gravity
non-inflammatory intact endothelium,
Inflammatory - Early endothelial contraction

Exudate = High protein content, high specific gravity.

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5
Q

What are they 3 types of exudate?

A 
Fibrinous  = high protein, few cells
Purulent = High protein, many cells
Sanguineous = high protein, blood
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6
Q

What are the mechanisms that can increase Vascular permeability?

A 
Endothelial contraction (Reversible) 
- Immediate and transient

Endothelial Retraction
- Delayed = develops in 4-6 hrs and sustained for 24+ hrs

Direct injury (non lethal) 
- Immediate or delayed but also sustained.
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7
Q

Endothelial cell contraction is mediated by what 4 things?

A

PAF
Histamine
Bradykinin
Leukotrienes

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8
Q

After Direct Endothelial injury, what mediates the increased vascular permeability?

A

Injurious agents
ROS/enzymes from PMN’s
*Endothelial cell retraction is mediated by IL-1 TNF and IFN-Y

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9
Q

What activates Endothelial cell retraction?

A

IL-1, TNF and IFN-Y

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10
Q

Activated Endothelial cells produce _______ and ______.

A

PGI2 and NO (vasodilation)

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11
Q

What molecule allows for transport of molecule out of blood vessel?

A

PECAM

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12
Q

What is the order of events Leukocyte migration? (5)

A
  1. Margination = Physical forces
  2. Rolling - selectins (speed bumps that slow molecules down) (weak, transient sticking)
  3. Adhesions - intergrins “Docking station” (ICAM and VCAM)
  4. Emigration or Transmigration - PECAM “Shuttle doors”
  5. Chemotaxis = movement alone the concentration gradient of chemotactic factors.
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13
Q

What are the steps of Phagocytosis?

A
  1. Recognition and attachment = Microbes bind to phagocyte receptors.
  2. Engulfment = Phagocyte membrane zips up around microbe.
  3. Killing and degradation
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14
Q

The presence of ______ defines acute inflammation.

A

Neutrophils (They release ROS and induce apoptosis)

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15
Q

What cell shows up after Neutrophils?

A

Monocytes and macrophages around day 3 (48hrs)

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16
Q

What are the functions of monocytes/macrophages?

A
  • phagocytosis
  • Cytokines
  • Antigen presentation
  • Plasma proteins
  • Enzymes
  • “Clear up mess the neutrophils made”
17
Q

What are other Inflammatory cells that turn up?

A

Lymphocytes = immune functions
Eosinophils = Allergic Reactions, parasites
Mast cells = histamine

18
Q

______ is diffuse tissue infiltration by PMN’S with Edema.

A

Cellulitis

19
Q

_____ is a localized collection of PMN’s or liquefactive necrosis (Pus)

A

Abscess

20
Q

How do features of Chronic inflammation differ from acute inflammation?

A 
Acute = days - weeks
Chronic = days - years
Acute = localized
Chronic = maybe systemic
Acute = no immune response
Acute = often reversible
21
Q

What are the 2 types of Chronic inflammation?

A

Non-specific
Granulomatous
*Tissue distraction leading to fibrosis (scarring) is common.

22
Q

What can cause Granulomatous inflammation?

A

Inorganic matter
Bacterial infections (like TB)
Parasitic infections (Toxoplasmosis)
Uncertain etiology

23
Q

What causes histamine release?

A

Physical injury Ag-IgE, C3a and C5a, Cytokines

24
Q

Prostaglandins are important for ______.

A

Vasodilation

25
Q

Thromboxane A2 is important for ________.

A

Vasoconstriction

26
Q

What are 3 important chemical inflammatory mediators?

A

Histamine releasers
Prostaglandins and Leukotrienes
Thromboxane A2

27
Q

What does Labile mean?

A

Continuously dividing (hematopoietic cells, surface epithelium)

28
Q

What does Stable refer to?

A

Tissue with some replicative activity (Parenchymal cells, smooth muscle cells, fibroblasts)

29
Q

What does Permanent refer to in wound healing?

A

non-proliferative tissue (Neurons, cardiac muscle)

30
Q

What are the effects of growth factors in wound healing?

A
  • Epithelial proliferation
  • Monocyte Chemotaxis
  • Fibroblast proliferation
  • Angiogenesis
  • collagen synthesis
31
Q

What is the primary cause of delayed healing?

A

Infection!

32
Q

What are other factors that affect wound healing?

A
  • nutrition
  • steroid therapy
  • mechanical factors
  • poor tissue perfusion

Pathology #1 (9 decks)

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