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SP16- Gen Path Exam 1 > Inflammation Overview > Flashcards

Inflammation Overview Flashcards

1
Q

Name the four typical signs of inflammation.

A

redness
swelling
heat
pain

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2
Q

How do formed cells communicate with the vasculature?

A

mediators

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3
Q

What are the two main events that occur with acute inflammation?

A
  1. Vascular changes + mediators

2. Cellular events + mediators

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4
Q

What are some common mediators that are present with acute inflammation?

A

IL-1
TNF-alpha
IL-6

“I Like, I Like TiNy, aCUTE things”

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5
Q

With acute inflammation there is a(n) ______ in vascular permeability.

A

increase

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6
Q

Increased vascular permeability will promote fluid leakage (edema) and cell accumulation. Which cells are the first to arrive at the site of injury?

A

PMNs

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7
Q

What are the effects of vasodilation?

A
  • relaxation of pre-capillary arterioles

- engorgement of capillary beds with redness/warmth

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8
Q

What are three mediators associated with vasodilation?

A

Nitric Oxide
Prostaglandins
Histamine

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9
Q

What is transudate?

A

a type of fluid that accumulates with inflammation

  • low protein
  • low specific gravity
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10
Q

How does exudate differ from transudate?

A

Exudate has a HIGH protein content and HIGH specific gravity

Transudate has a LOW protein content and LOW specific gravity

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11
Q

Is exudate associated with “early endothelial contraction?”

A

NO, exudate is seen later.
*transudate is associated with early endothelial contraction in the case of inflammatory processes: the endothelium contracts but is still intact (not separating)

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12
Q

True or False: Transudate can be inflammatory or non-inflammatory.

A

True

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13
Q

What are three forms of exudate?

A
  1. Fibrinous
  2. Purulent
  3. Sanguineous
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14
Q

Describe fibrinous exudate.

A

high protein

few cells

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15
Q

Describe purulent exudate.

A 
high protein
many cells (PMNs)
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16
Q

Describe sanguineous exudate.

A

high protein

presence of blood

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17
Q

In a normal vessel, the hydrostatic pressure is slightly higher but relatively equal to the ________.

A

colloid osmotic pressure

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18
Q

Transudate is associated with an increase in ______ pressure.

A

hydrostatic pressure (plus decreased colloid osmotic pressure=fluid leakage)

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19
Q

What are the three mechanisms of increased vascular permeability?

A
  1. Endothelial contraction
  2. Endothelial retraction
  3. Direct injury
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20
Q

Which mechanism of increased vascular permeability is delayed (develops in 4-6 hours) and sustained for 24 hours or more?

A

Endothelial REtraction

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21
Q

Which mechanism of vascular permeability occurs immediately and is reversible?

A

Endothelial CONtraction

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22
Q

Which mechanism of vascular permeability is either immediate OR delayed and is sustained?

A

Direct injury (detachment/necrosis/non-lethal injury)

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23
Q

Endothelial ________ is mediated by PAF, histamine, bradykinin, and leukotrienes.

A

CONtraction

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24
Q

Endothelial ________ is mediated by IL-1, TNF, and IFN-gamma.

A

REtraction

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25
Endothelial ________ is mediated by ROS/enzymes from PMNs.
injury
26
Pain symptoms of acute inflammation are mediated by _____ and ______.
bradykinin PGE2 "P and B: P-ain is B-ad"
27
Fever from acute inflammation is mediated by _____, ______, and _____.
IL-1 TNF PGE2 "fever P.I.T"
28
True or False: Infectious agents, hypoxia, and inflammatory mediators will activate endothelial cells.
True
29
Do "activated endothelial cells" increase or decrease the expression of adhesion molecules?
increase
30
Activated endothelial cells will produce PGI2 and ______ which results in vasodilation.
Nitric Oxide (NO)
31
What are the five leukocyte actions that follow activation?
1. Margination 2. Rolling 3. Adhesion 4. Transmigration 5. Chemotaxis
32
Which mediators are involved in leukocyte rolling?
selectins
33
Which two integrins are involved in leukocyte adhesion?
ICAM | VCAM
34
________ is integral to leukocyte emigration or transmigration (allows neutrophils to pass through gaps in endothelial cells)
PECAM
35
Cellulitis is caused by ______ cells moving into tissues.
White Blood
36
What are the four stages of phagocytosis/digestion?
1. Attachment 2. Engulfment 3. Degranulation 4 Oxidative burst
37
Oxidative burst occurs within a ________.
phagolysosome
38
True or False: There are multiple mechanisms of intracellular killing by leukoctyes that are non-respiratory.
True | ex. lysozyme, major basic protein, defensins, bactericidal permeability-increasing protein
39
The presence of _____ defines acute inflammation.
neutrophils
40
What cell type is responsible for apoptosis, responds to necrosis, and releases ROS?
neutrophil
41
Edema activity peaks after ______ hours.
10 to 12 (then drops)
42
PMN activity peaks after ______ hours.
24 hours (then drops)
43
Macrophage/Monocyte activity peaks after ______ and then remains within tissue for _____.
2 to 3 days | months
44
What are the functions of activated macrophages?
- P hagocytosis - R OS - A ntigen presentation - N itric Oxide and prostaglandins - C ytokines and plasma proteins - E nzymes and factors of healing/repair "They PRANCE in to clean up the mess"
45
What are the three "later stage" inflammatory cells?
``` lymphocytes (immune function) eosinophils (allergy, parasite) mast cells (histamine) ```
46
What are the three different patterns of inflammation?
1. Abscess 2. Cellulitis 3. Ulcer
47
What is cellulitis?
diffuse tissue infiltration by PMNs, with edema
48
What is an abscess?
a LOCALIZED collection of PMNs and degradation of tissues (liquefactive necrosis: center filled with pus)
49
What is an ulcer?
erosion of epithelium with exposure to the underlying connective tissue
50
Compare the duration of acute inflammation to that of chronic inflammation.
Acute: days - weeks Chronic: days - years
51
What is the location of acute inflammation?
localized
52
What is the location of chronic inflammation?
maybe systemic
53
Is there an immune response for acute inflammation?
No
54
Is there an immune response for chronic inflammation?
Yes
55
Is acute inflammation reversible? Chronic?
Acute: often reversible Chronic: maybe
56
Which cells are most prevalent in acute inflammation?
PMNs
57
Which cells are most prevalent in chronic inflammation?
macrophages and lymphocytes
58
What are the two types of chronic inflammation?
1. non-specific | 2. granulomatous
59
True or False: Tissue destruction leading to fibrosis is common in chronic inflammation.
True
60
What is another (more common) name for "fibrosis?"
scarring
61
_______ is a common cause of chronic inflammation.
Infection (Tuberculosis)
62
Why is acute inflammation of the lung more life threatening than chronic inflammation of the lung?
the alveoli fill with PMNs
63
Which cells of chronic inflammation are seen histologically as "mostly nucleus?"
lymphocytes
64
Which cells of chronic inflammation are seen with "eccentric nuclei?"
plasma cells
65
Which cells of chronic inflammation are filled with many small red granules?
eosinophils
66
What are the four causes of granulomatous (chronic type) inflammation?
1. Inorganic matter (sutures) 2. Bacterial infection (TB) 3. Parasitic infection (toxoplasmosis) 4. Uncertain etiology (sarcoidosis, Crohn's disease)
67
Which inflammatory mediators will increase vascular permeability? (5)
``` histamine bradykinin leukotrienes PAF Complements C5a and C3a ```
68
Which three mediators are involved in vasodilation?
histamine NO Prostaglandins
69
Which mediators are involved in chemotaxis/opsonization?
C5a and C3a PAF Leukotriene B4
70
Which chemical mediators are highly involved with pain potentiation?
bradykinin prostaglandins IL-1 TNF
71
Which chemical mediators increase fever associated with inflammation?
IL-1 TNF Prostaglandins
72
Prostaglandins will vasodilate; whereas, its opposite _______ will vasoconstrict.
Thromboxane A2
73
Prostaglandins and leukotrienes are derived from ______.
arachidonic acid - ->cyclo-oxygenase = prostaglandins - ->lipoxgenase = leukotrienes
74
What is a "labile" cell? Give examples.
continuously dividing (regrowable) * hematopoietic cells * surface epithelium
75
What is a "stable" cell? Give examples.
some replicative activity * parenchymal cells * smooth muscle cells * fibroblasts
76
What is a "permanent" cell? Give examples.
nonproliferative, not regenerative * neurons * cardiac muscle
77
First Intention healing occurs within ______ days.
3 to 5
78
Second Intention healing occurs within _______, and is accompanied by _______ shrinkage.
1 to 3 weeks | myofibroblastic
79
_______ effect wound healing such as: epithelial proliferation, monocyte chemotaxis, fibroblast proliferation, angiogenesis, collagen synthesis
Growth Factors
80
What is the primary cause of delayed wound healing?
infection
81
Other than infection, what are some additional factors that would affect wound healing?
- nutrition - steroid therapy - mechanical factors - poor tissue perfusion (diabetes, atherosclerosis)

SP16- Gen Path Exam 1 (10 decks)

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