Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Patho Exam 4 > Park:Acute and Chronic Inflammation > Flashcards

Park:Acute and Chronic Inflammation Flashcards

1
Q

When does inflammation occur?

A

In response infections or noxious stimuli (injuries, foreign body, burn, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the purpose of inflammation?

A

-to eliminate harmful agents (microbes, toxins) and necrotic cells
-initiate the healing process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How could inflammation injure normal tissues?

A

-a inflammation response may be too strong (think severe infection)
-the response may be prolonged (persistent or recurrent infection)
-inappropriate response may be occurring (self-antigens in autoimmune diseases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some pharmacologic approaches to inflammation?

A

-glucocorticoids
-NSAIDs
-antihistamines
-leukotriene antagonists
-biologics targeting cytokine signaling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are leukocytes

A

white blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phagocytes

A

a cell capable of engulfing and absorbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are types of phagocytes

A

-neutrophils
-mast cells
-macrophages
-monocytes
-dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Granulocytes

A

an immune cell that has granules with enzymes that are released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are types of granulocytes?

A

-neutrophils
-eosinophils
-basophils
-mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lymphocytes

A

responsible for producing antibodies and regulating immune respose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are types of leukocytes?

A

-B cells
-T cells
-Natural killer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Innate immunity

A

-nonspecific
-fast response (0-4 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Adaptive immunity

A

-specific
-slow response (4-14 days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Acute inflamation

A

-rapid onset
-short duration (minutes to days)
-accumulation of fluid and plasma proteins (exudation)
-accumulation of neutrophils
-tumor necrosis factor (TNF)
-interleukin-1 (IL-1)
-chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic inflammation

A

-insidious
- longer duration (months to years)
-tissue destruction by inflammatory cells
-vascular proliferation
-fibrosis (scarring)
-influx of lymphocytes and macrophages
-interferon-y (IFN-y) by T cells and interleukin-12 by macrophages (synergistic stimulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain how an acute inflammatory response happens

A

-Upon tissue damage or introduction of bacteria histamines are released increasing blood flow to the area
-histamines cause capillaries to leak, releasing phagocytes and clotting factors into the wound
-phagocytes engulf bacteria, dead cells, and cellular debris
-platelets move out of the capillary to seal the wounded area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the acute inflammatory response?

A
  • phagocytes in tissue recognize offending agents and liberate chemical mediators of inflammation
    -chemical mediators widen blood vessels (vasodilation) and increase their permeability in the vicinity
    -plasma and circulating leukocytes diffuse to the location of the offending agent (leukocyte recruitment)
    -activated leukocytes remove the offending agents (phagocytosis)
    -leukocytes produce signaling molecules that suppress inflammation (eg. lipoxins)
    -the damaged tissue is repaired (cell proliferation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are characteristics of acute inflammation?

A

-heat (calor)
-redness (rubor)
-swelling (tumor)
-pain (dolor)
-loss of function (functio laesa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the major components of inflammation?

A

-vascular stage
-cellular stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is involved in the vascular stage?

A

-vasodilation
-increased permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is involved in the cellular stage?

A

-leukocyte recruitment
-phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does an increase in vascular diameter (vasodilation) cause?

A

-decrease in fluid velocity
-increase in viscosity (due to fluid loss to tissues)
-increased leukocyte setting along the inner surface of the blood vessels (margination)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What can cause an increase in vascular permeability?

A

-gaps due to endothelial contraction which is the most common mechanism (caused by histamine, leukotrienes, bradykinin)
-increased fluid flow through endothelial cells (transcytosis)
-direct endothelial (traumatic) trauma
-leukocyte-dependent endothelial cell damage/death due to release of toxic mediators by leukocytes
-leakage from new blood vessels that form at the site of injury (thinner)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are vascular changes

A

-transudate
-exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Transudate
-increased hydrostatic pressure (venous outflow obstruction, ex congestive heart failure) OR -decreased colloid osmotic pressure (decreased protein synthesis, ex liver disease; increased protein loss; ex kidney disease) -results in small holes, release of plasma with little proteins and no cells (water) -example is edema...accumulation of fluid and swelling at site of inflammation (can happen without inflammation as well)
26
Exudate
-inflammation triggers fluid and protein leakage, vasodilation and stasis, and increased interendothelial spaces -has bigger holes with allows protein rich fluid with numerous cells to exit
27
How are leukocytes recruited?
-margination -loose attachment and rolling (selectins) -adhesion (integrins) -transmigration -chemotaxis
28
Chemotaxis can be caused by what?
-bacterial products (ex lipopolysaccharides (LPS)) -chemokines -complement system (C5a) -leukotriene B4 (LTB4)
29
How is phagocytosis initiated?
-direct recognition -indirect recognition by opsonins
30
How does direct phagocytosis recognition occur?
-direct recognition of microbes by pattern recognition receptors such as toll like receptors (lipopolysaccharides, flagellin, etc) or mannose receptors (outer membrane of bacteria)
31
How does indirect phagocytosis recognition occur?
-opsonins such as IgG, C3b, and collectins (carbohydrate-binding lectins) coat the foreign body and dead cells in a process known as opsonization...specific receptors on phagosomes then recognize the opsonins (Fc or C3b receptors)
32
How does engulfment occur in phagocytosis?
-the receptors on the opsonin or microbe is recognized (receptor mediated endocytosis) -this triggers the pseudopods (arms) to extend around the foreign body and form a phagosome
33
How does a phagocytosis kill foreign bodies?
-the phagosome fuses with a lysosome (phagolysosome) -lysosomal degradation then occurs through the digestive enzymes and defensins within the lysozyme -the digested particles are then released, the toxic nitrogen and oxygen compounds (oxidative burst)
34
What types are mediators are found in acute inflammation?
-plasma derived mediators -cell-derived mediators
35
What are cell derived mediators
-histamine -platelet activating Factor (PAF)
36
Histamine
-first mediator released upon acute inflammation but transient -binds to histamine type 1 receptors on endothelial cells and causes vasodilation and increases vascular permeability -H1 receptor antagonist are used as antihistamine drugs
36
Platelet activating factor (PAF)
-generated from phospholipids by phospholipase A2 -induces platelet aggregation -100~1000x more potent than histamine in inducing inflammation reactions
36
What happens with the cleaved fatty acid fro the phospholipid that was cleaved by phospholipase A2?
It becomes an eicosanoid
36
What do eicosanoids trigger?
two pathways -cyclooxygenase (COX) pathway -lipoxygenase pathway
36
eicosanoids
-derived from polyunsaturated fatty acids -ex is arachidonic acid (has 20 carbons)
37
What can inhibit the COX pathway?
-aspirin -NSAIDs
37
What does the COX pathway lead to?
-generation of prostaglandins (complex inflammatory responses including fever and pain) -generation of thromboxane (causes vasoconstriction and platelet aggregation)
37
What are examples of plasma protein mediators?
-thrombin and fibrinopeptides -C3a, C5a, C3b -bradykinin
37
What can inhibit eicosanoid from triggering the COX pathway and lipoxygenase pathway?
corticosteroid medications
37
What does the lipoxygenase pathway lead to?
generation of leukotrienes (similar to histamine but are more potent and long acting; significant contributors to allergic reactions)
38
What are thrombin and fibrinopeptides apart of?
the clotting system
39
What does thrombin activate?
leukocytes
40
what are fibrinopeptides produced from?
the digestion of fibrinogen by thrombin
41
What do fibrinopeptides do?
-Increase vascular permeability -chemotactic
42
What are C3a, C5a, C3b?
-a compliment system, they work together
43
what does the letter indicate on C3a, C5a, C3b?
that they have been cleaved
44
what does C3a and C5a do?
increase vascular permeability and cause vasodilation
45
what does C5a do?
-activate leukocytes -chemotactic
46
What does C3b do?
acts as an opsonin
47
What is bradykinin apart of?
the kinin system
48
How is bradykinin formed?
By the cleavage of kininogens by protease called kallikrenins
49
what does bradykinin do?
-increases vascular permeability -cause vasodilation -cause pain
50
What pathway activates the plasma protein mediators?
The Factor X11 (Hageman factor) pathway
51
cytokine
-small proteins that are part of the immune systems signaling network -essential for regulating the immune system
52
Cytokine secretion is___
-transient -tightly regulated
53
What types of functions do cytokines have?
-pleiotropic -redundant
54
What are the major cytokines that mediate the acute inflammation pathway?
-TNF -IL-1
55
What is the major source of TNF and IL-1 cytokine production?
activated macrophages
56
What types of responses can the cytokines TNF and IL-1 generate?
-cellular -systemic
57
what are chemokines?
-chemotactic cytokines -they recruit and direct the migration of immune and inflammatory cells -they generate a persistent chemotactic gradient
58
Nitric Oxide
-synthesized by inducible nitric oxide synthase (iNOS) which is induced by inflammatory cytokines and mediators -short-lived (a few seconds) -locally acting
59
What does Nitric Oxide (NO) do?
-triggers the relaxation of vascular smooth muscles by vasodilation -works as an antimicrobial agent in activated macrophages
60
Reactive oxygen species (ROS)
-synthesized by NADH oxidase pathway -short lived -locally acting
61
What happens to ROS?
-released extracellularly by neutrophils and macrophages after stimulation -may cause tissue injury
62
How can lysosomal proteases cause tissue injury?
the release into the extracellular space can lead to matrix degradation and destructive tissue injury
63
What causes the release of lysosomal proteases?
-premature degranulation of lysosomes -phagocytosis attempts of large, flat surfaces (frustrated phagocytosis) -damage of leukocytes (ex. urate crystals in gout)
64
What antiproteases are present to inhibit lysosomal proteases?
- a2-macroglobulin -a1-antitrypsin -all exist in the serum and extracellular matrix
65
What mediators cause vasodilation and increased vascular permeability?
-Histamine -PAF -C3a and C5a -bradykinin -leukotrienes (LTC,LTD, LTE) -prostaglandins -NO
66
what mediators are involved in chemotaxis?
-C5a -leukotriene B (LTB) -bacterial products (LPS) -chemokine
67
what mediators cause fever?
-IL-1 -Il-6 -TNF -prostaglandins
68
what mediators cause pain?
-prostaglandins -bradykinin
69
what mediators cause tissue damage?
-lysosomal enzymes -reactive oxygen species -nitric oxide
70
Abscess
- a localized area of inflammation containing a purulent exudate (pus) that may be surrounded by a neutrophil layer -caused by excessive neutrophil infiltrates or certain bacterial/fungal infections (pyogenic)
71
Ulceration
-a site of inflammation where an epithelial surface has become necrotic and eroded -may occur as the result of traumatic injury to the epithelial surface (peptic ulcer) or vascular compromise (foot ulcers associated with diabetes)
72
What is chronic inflammation?
inflammation of prolonged duration (weeks to months to year)
73
What happens during chronic inflammation?
active inflammation, tissue injury, and healing occur simultaneously ( a cycle)
74
what can happen if acute inflammation is unresolved?
it can progress to chronic inflammation
75
What are characteristics of chronic inflammation?
-infiltration with mononuclear ("chronic inflammatory") cells (macrophages, lymphocytes, and plasma cells) -tissue destruction -repair involving new vessel proliferation (angiogenesis) and fibrosis (scarring)
76
What are some causes of chronic inflammation?
-viral infection (intracellular) -persistent microbial infection (delayed hypersensitivity) -prolonged exposure to toxic agents (silica in lungs) -autoimmune diseases (RA/ MS
77
Where are chronic inflammation macrophages from?
-derived from circulating blood monocytes -activated by cytokines, bacterial products, mediators of inflammation, dead cells, etc
78
what are chronic inflammation macrophages alos known as?
epithelioid macrophages
79
What products released by epithelioid macrophages may cause tissue damage?
-proteases -complement components, coagulation factors -ROS -NO -eicosanoids -cytokines -growth factors (leads to fibrosis)
80
What happens to macrophages in chronic inflammation
macrophage accumulation persists
81
Explain the reciprocal relationship of lymphocytes and macrophages
- lymphocytes are activated by macrophage presenting antigen fragments -activated lymphocytes release mediators including interferon- y (IFN-y) -IFN-y activates macrophages -activated macrophages release cytokines including IL-12 -IL-12 further activates lymphocytes
82
What happens between macrophages and lymphocytes
they persistently stimulate one another until the triggering antigen is removed
83
what is also present in chronic inflammation (besides macrophages)
-plasma cells -eosinophils -mast cells
84
What in granulomatous inflammation
- a distinctive form of chronic inflammation -formation of granuloma
85
What is a granuloma
a small (1-2 mm) lesion of epitheliod macrophages surrounded by lymphocytes
86
what causes granulomas?
-offending agents not easily controlled by other inflammatory mechanisms such as foreign bodies (splinters, sutures, silica, and asbestos) or microorganisms (cause tuberculosis, syphilis, sarcoidosis, deep fungal infections, and brucellosis)
87
What are foreign body giant cells?
-multi-nucleated cells formed by coalesced macrophages -encapsulate and isolate the offending agents
88
what are the two cell types most responsible for chronic inflammation A. macrophages and lymphocytes B. neutrophils and lymphocyte C. basophils and lymphocytes D. neutrophils and macrophages E. basophils and macrophages
A. macrophages and lymphocytes
89
Which of the following does not belong to the classic signs of inflammation? A. heat B. redness C. swelling D. scarring E. pain
D. scarring
90
The vascular change upon inflammation increases leukocyte setting along the surface of the blood vessels, which is called____ A. transcytosis B. edema C. extravasation D. vasodilation E. margination
E. margination
91
which of the following plasma proteins causes pain? A. C3b B. fibrinopeptides C. C3a and C5a D. bradykinin E. thrombin
D. bradykinin
92
The mediators of inflammation are matched with the enzyme responsible for their production. Which pair is incorrect? A. Nitric oxide (NO)- inducible nitric oxide synthase (iNOS) B. platelet activating factor (PAF)- phospholipase A2 C. bradykinin- kallikrein D. leukotrienes- cyclooxygenase E. fibrinopeptides-thrombin
D. leukotrienes-cyclooxygenase
93
What are the key cytokines responsible for acute inflammation? A. IFN-y and IL-12 B. IFN-y and TNF C. TNF and IL-12 D. IFN-y and IL-1 E. TNF and IL-1
E. TNF and IL-1
94
Which of the following mediators may cause tissue damage? A, lysosomal enzymes B. Reactive oxygen species (ROS) C.Nitric Oxide (NO) D. all of the above E. none of the above
D. all of the above
95
Which of the following is not responsible for killing of the engulfed bacteria in phagolysosomes? A. defensins B. Hypochlorous radical C.a2-macroglobulin D. Lysosomal proteases E. hydrogen peroxide
C. a2- macroglobulin
96
What cells are commonly found in granulomas? A. cancer cells and neutrophils B. cancer cells and lymphocytes C. epithelioid macrophages and lymphocytes D. epithelioid macrophages and neutrophils E. neutrophils and lymphocytes
C. epithelioid macrophages and lymphocytes
97
What do pattern recognition receptors of leukocytes recognize directly A. chemokine B. microbes C. histamines D. opsonins E. selectins and integrins
B. microbes

Patho Exam 4 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions