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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
Q

Endothelial ________ is mediated by ROS/enzymes from PMNs.

A

injury

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26
Q

Pain symptoms of acute inflammation are mediated by _____ and ______.

A

bradykinin
PGE2

“P and B: P-ain is B-ad”

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27
Q

Fever from acute inflammation is mediated by _____, ______, and _____.

A

IL-1
TNF
PGE2

“fever P.I.T”

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28
Q

True or False: Infectious agents, hypoxia, and inflammatory mediators will activate endothelial cells.

A

True

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29
Q

Do “activated endothelial cells” increase or decrease the expression of adhesion molecules?

A

increase

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30
Q

Activated endothelial cells will produce PGI2 and ______ which results in vasodilation.

A

Nitric Oxide (NO)

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31
Q

What are the five leukocyte actions that follow activation?

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration
  5. Chemotaxis
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32
Q

Which mediators are involved in leukocyte rolling?

A

selectins

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33
Q

Which two integrins are involved in leukocyte adhesion?

A

ICAM

VCAM

34
Q

________ is integral to leukocyte emigration or transmigration (allows neutrophils to pass through gaps in endothelial cells)

A

PECAM

35
Q

Cellulitis is caused by ______ cells moving into tissues.

A

White Blood

36
Q

What are the four stages of phagocytosis/digestion?

A
  1. Attachment
  2. Engulfment
  3. Degranulation
    4 Oxidative burst
37
Q

Oxidative burst occurs within a ________.

A

phagolysosome

38
Q

True or False: There are multiple mechanisms of intracellular killing by leukoctyes that are non-respiratory.

A

True

ex. lysozyme, major basic protein, defensins, bactericidal permeability-increasing protein

39
Q

The presence of _____ defines acute inflammation.

A

neutrophils

40
Q

What cell type is responsible for apoptosis, responds to necrosis, and releases ROS?

A

neutrophil

41
Q

Edema activity peaks after ______ hours.

A

10 to 12 (then drops)

42
Q

PMN activity peaks after ______ hours.

A

24 hours (then drops)

43
Q

Macrophage/Monocyte activity peaks after ______ and then remains within tissue for _____.

A

2 to 3 days

months

44
Q

What are the functions of activated macrophages?

A
  • 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
Q

What are the three “later stage” inflammatory cells?

A 
lymphocytes (immune function)
eosinophils (allergy, parasite)
mast cells (histamine)
46
Q

What are the three different patterns of inflammation?

A
  1. Abscess
  2. Cellulitis
  3. Ulcer
47
Q

What is cellulitis?

A

diffuse tissue infiltration by PMNs, with edema

48
Q

What is an abscess?

A

a LOCALIZED collection of PMNs and degradation of tissues (liquefactive necrosis: center filled with pus)

49
Q

What is an ulcer?

A

erosion of epithelium with exposure to the underlying connective tissue

50
Q

Compare the duration of acute inflammation to that of chronic inflammation.

A

Acute: days - weeks
Chronic: days - years

51
Q

What is the location of acute inflammation?

A

localized

52
Q

What is the location of chronic inflammation?

A

maybe systemic

53
Q

Is there an immune response for acute inflammation?

A

No

54
Q

Is there an immune response for chronic inflammation?

A

Yes

55
Q

Is acute inflammation reversible? Chronic?

A

Acute: often reversible
Chronic: maybe

56
Q

Which cells are most prevalent in acute inflammation?

A

PMNs

57
Q

Which cells are most prevalent in chronic inflammation?

A

macrophages and lymphocytes

58
Q

What are the two types of chronic inflammation?

A
  1. non-specific

2. granulomatous

59
Q

True or False: Tissue destruction leading to fibrosis is common in chronic inflammation.

A

True

60
Q

What is another (more common) name for “fibrosis?”

A

scarring

61
Q

_______ is a common cause of chronic inflammation.

A

Infection (Tuberculosis)

62
Q

Why is acute inflammation of the lung more life threatening than chronic inflammation of the lung?

A

the alveoli fill with PMNs

63
Q

Which cells of chronic inflammation are seen histologically as “mostly nucleus?”

A

lymphocytes

64
Q

Which cells of chronic inflammation are seen with “eccentric nuclei?”

A

plasma cells

65
Q

Which cells of chronic inflammation are filled with many small red granules?

A

eosinophils

66
Q

What are the four causes of granulomatous (chronic type) inflammation?

A
  1. Inorganic matter (sutures)
  2. Bacterial infection (TB)
  3. Parasitic infection (toxoplasmosis)
  4. Uncertain etiology (sarcoidosis, Crohn’s disease)
67
Q

Which inflammatory mediators will increase vascular permeability? (5)

A 
histamine
bradykinin
leukotrienes
PAF
Complements C5a and C3a
68
Q

Which three mediators are involved in vasodilation?

A

histamine
NO
Prostaglandins

69
Q

Which mediators are involved in chemotaxis/opsonization?

A

C5a and C3a
PAF
Leukotriene B4

70
Q

Which chemical mediators are highly involved with pain potentiation?

A

bradykinin
prostaglandins
IL-1
TNF

71
Q

Which chemical mediators increase fever associated with inflammation?

A

IL-1
TNF
Prostaglandins

72
Q

Prostaglandins will vasodilate; whereas, its opposite _______ will vasoconstrict.

A

Thromboxane A2

73
Q

Prostaglandins and leukotrienes are derived from ______.

A

arachidonic acid

  • ->cyclo-oxygenase = prostaglandins
  • ->lipoxgenase = leukotrienes
74
Q

What is a “labile” cell? Give examples.

A

continuously dividing (regrowable)

  • hematopoietic cells
  • surface epithelium
75
Q

What is a “stable” cell? Give examples.

A

some replicative activity

  • parenchymal cells
  • smooth muscle cells
  • fibroblasts
76
Q

What is a “permanent” cell? Give examples.

A

nonproliferative, not regenerative

  • neurons
  • cardiac muscle
77
Q

First Intention healing occurs within ______ days.

A

3 to 5

78
Q

Second Intention healing occurs within _______, and is accompanied by _______ shrinkage.

A

1 to 3 weeks

myofibroblastic

79
Q

_______ effect wound healing such as: epithelial proliferation, monocyte chemotaxis, fibroblast proliferation, angiogenesis, collagen synthesis

A

Growth Factors

80
Q

What is the primary cause of delayed wound healing?

A

infection

81
Q

Other than infection, what are some additional factors that would affect wound healing?

A
  • nutrition
  • steroid therapy
  • mechanical factors
  • poor tissue perfusion (diabetes, atherosclerosis)

SP16- Gen Path Exam 1 (10 decks)

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