Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PATHO > Lecture 3+4: Acute and Chronic Inflammation > Flashcards

Lecture 3+4: Acute and Chronic Inflammation Flashcards

1
Q

Inflammation

A

-from infections or bad stimuli
-eliminates harmful agents and necrotic cells
-initiates healing
-may injure normal tissues

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

Inflammation damaging normal tissue scenarios

A

-response too strong (severe infection)
-prolonged reponse (persistent or recurrent infection)
-inappropriate response (self antigens in autoimmune disease)

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

pharmacological 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
4
Q

leukocytes

A

white blood cells

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

phagocytes

A

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

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

Granulocytes

A

-neutrophils
-eosinophils
-basophils
-mast cells

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

lymphocytes

A

-B cells
-T cells
-NK cells

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

Acute inflammation

cell types
cytokines

A

-rapid onset
-short duration
-exudation
-accumulation of NEUTROPHILS
-TNF and IL-1 and chemokines

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

exudation

A

accumulation of fluid and plasma proteins

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

Chronic inflammation

cell type
cytokines

A

-insidious and longer (months to years)
-tissue destroyed by inflammatory cells
-scarring
-influx of LYMPHOCYTES and MACROPHAGES
-IFN-y by T cells and IL-12 by macrophages (synergistic stimulation)

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

scarring

A

vascular proliferation and fibrosis

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

Acute Inflammatory response

A
  1. Phagocytes recognize threat then release chemical mediators of inflammation
  2. mediators cause vasodilation and increase permeability
  3. leukocytes diffuse to site
  4. Phagocytosis by leukocytes
  5. Luekocyte sends signals that suppress inflammation (lipoxins)
  6. Damage tissue is repaired (cell proliferation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Signs of acute inflammation

A

-heat
-redness
-swelling
-pain
-loss of function

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

Major components of inflammation

A

-vascular stage
-cellular stage

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

vascular stage of inflammation

A

-vasodilation
-increased permeability

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

cellular stage of inflammation

A

-leukocyte recruitment
-phagocytosis

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

Vasodilation

A

-decrease in fluid velocity
-increased viscosity due to fluid loss to tissues
-margination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

margination

A

-increased leukocyte settling along the inner surface of blood vessels

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

Increase in vascular permeability

A

-Gaps due to endothelial contraction (histamine, leukotrienes, bradykinin)
-increased fluid flow through endothelial cells (transcytosis)
-direct endothelial *traumatic) injury
-leukocyte-dependent endothelial cell damage due to release of toxic mediators by leukocytes
-leakage from new blood vessels that form at site of injury

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

Vascular changes

A

-transudate
-exudate
-edema

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

transudate

A

-small holes
-plasma with little protein
-no cells

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

exudate

A

-bigger holes
-protein rich fluid
-numerous cells

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

edema

A

-accumulation of fluid and swelling at site of inflammation

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

Leukocyte recruitment

A

-margination
-rolling (selectins)
-adhesion (integrins)
-transmigration
-chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Chemotaxis

A

-bacterial products (LPS)
-chemokines
-complement system
-leukotriene B4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Phagocytosis steps

A
  1. recognition (direct or indirect)
    2, engulfment
  2. Killing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Direct recognition in phagocytosis

A

-by pattern recognition receptors
-toll-like receptors (LPS, flagella)
-mannose receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Indirect recognition in phagocytosis

A

-by opsonins (IgG, C3b, collectins)
-opsonization
-specific receptors recognize opsonins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

opsonization

A

coat foreign body and dead cells

30
Q

Engulfment step of phagocytosis

A

-receptor-mediated ENDOcytosis
-psuedopods form PHAGOSOME around foreign body

31
Q

Intracellular killing phase of phagocytosis

A

-phagolysosome
-lysosomal degradation
-oxidative burst

32
Q

Histamine

A

-first mediator of inflammation released upon acute inflammation, but transient
-binds H1 receptors
=vasodilation and increased permeability

33
Q

antihistamine drugs

A

H1 receptor antagonists

34
Q

Platelet activating factor (PAF)

A

-mediator of inflammtion
-generated from phospholipids by phospholypase A2
-induces platelet aggregation
-100-10000 times more potent than histamine

35
Q

Eicosanoids

A

-derived from polyunsat FAs like arachidonic acid
-COX pathway (prostaglandins and thromboxane)
-Lipoxygenase pathway (leukotrienes)

36
Q

prostaglandins

A

-complex inflammatory response
-fever and pain

37
Q

thromboxane

A

-vasoCONSTRICTION
-platelet aggregation
-INHIBITED by NSAIDs

38
Q

NSAIDs inhibt

A

thromboxane part of COX pathway

39
Q

leukotrienes

A

-similar to histamine
-more potent and longer
-significant in allergic reactions

40
Q

Plasma proteins

A
  1. clotting system: thrombin and fibrinopeptides
  2. complement system: C3a, C5a, C3b
  3. kinin system: bradykinin
41
Q

thrombin

A

activates leukocytes

42
Q

fibrinopeptides

A

-increase permeability
-chemotactic
-produced from digestion of fibrinogen bu thrombin

43
Q

Anaphylatoxins

A

-C3a and C5a
-vasodilation
-increase permeability

44
Q

C5a

A

-activates leukocytes
-chemotactic

45
Q

C3b

A

-acts as opsonin

46
Q

Bradykinin

A

-vasodilation
-increased permeability
-causes PAIN
-formed by cleavage of kininogens by protease killikreins

47
Q

Cytokines

A

-secretion is transient and tightly regulated
-pleiotropic and redundant functions
-TNF-a and IL-1
-chemokines

48
Q

TNF-a and IL-1

A

-major cytokines of inflammation
-come from activated macrophages
-generate cellular and systemic responses

49
Q

Chemokines

A

-chemotactic cytokines
-recruit cells
-generate persistant chemotactic gradient

50
Q

Nitric Oxide (NO)

A

-short lived (sec) locally acting
-synthesized by inducible nitric oxide synthase (iNOS) which is induced by inflammatory cytokines and mediators
-vasodilation
-antimicrobial in activated macrophages

51
Q

Reactive Oxygen Species (ROS)

A

-short lived
-from NADH oxidase pathway
-superoxide, hydrogen peroxide, hydroxyl radical
-released extracellularly by neutrophils and macrophages after stimulation
-may cause tissue injury

52
Q

Injury by Lysosomal proteases

A

-release of lysosomal contents into EXTRAcellular space
-matrix degradation and tissue injury

53
Q

causes of injury by lysosomal protease

A

-premature degranulation of lysosomes
-phagocytosis attempts of large, flat surfaces (frustrated phagocytosis)
-damage of leukocytes (urate crystals in gout)

54
Q

Antiproteases

A

-inhibit lysosomal proteases
-a2-macroglobulin, a1-antitrypsin
-exist in serum and extracellular matrix

55
Q

Vasodilation and increased vascular permeability is caused by:

A

-histamine
-PAF
-C3a and C5a
-Bradykinin
-leukotrienes (LTC, LTD, LTE)
-prostaglandins
-Nitric oxide

56
Q

Chemotaxis caused by:

A

-C5a
-Leukotriene B (LTB)
-bacterial products (LPS)
-chemokines

57
Q

Fever caused by:

A

-IL-1
-IL-6
-TNF-a
-prostaglandins

58
Q

Pain caused by:

A

-prostaglandins
-bradykinin

59
Q

tissue damage caused by:

A

-lysosomal enzymes
-ROS
-nitric oxide

60
Q

Abscess

A

-localized area of inflammation
-pus that may be surrounded by neutrophils
-excessive neutrophil infiltrates or certain bacterial/fungal pyogenic infections

61
Q

Ulceration

A

-site of inflammation where epithelial surface has become necrotic and eroded
-may occur as result of tramatic injury to epithelial surface (peptic) or vascular compromise (foot ulcers from diabetes)

62
Q

Chronic inflammation

A

-weeks to years
-inflammation, injury, and healing occur at same time
-may progress from unresolved acute inflammation

63
Q

Characteristics of chronic inflammation

A

-infiltration with mononuclear cells: macrophages, lymphocytes, plasma cells
-tissue destruction
-repair involving new vessel proliferation (angiogenesis) and fibrosis

64
Q

Causes of chronic inflammation

A

-viral infection intracellular
-persistant infection (delayed hypersensitivity)
-prolonged exposure to toxins
-autoimmune disease

65
Q

Epithelioid macrophages

A

-activated by cytokines, bacterial products, mediators, dead cells, etc
-release products that may cause tissue damage
-macrophage accumulation persists

66
Q

Macrophages release:

A

-proteases
-complement, coagulation factors
-ROS and NO
-eicosanoids
-cytokines
-growth factors = fibrosis

67
Q

Lymphocytes

A

-reciprocal of macrophage
1. activation by macrophage presenting antigen
2. activated lymphocytes release mediators (IFN-y)
3. IFN-y activates macrophages
4. activated macrophages release cytokines (IL-12)
5. IL-12 activates lymphocytes

68
Q

Cells in chronic inflammation

A

-macrophages and lymphocytes stimulate each until the antigen is gone
-also plasma, eosinophils, and mast cells

69
Q

Granulomatous Inflammation

A

-form of chronic inflammation
-formation of granuloma
-caused by hard to control agents
-foreign bodies
-micros that cause TB, syphilis, sarcoidosis, deep fungal infections, brucellosis

70
Q

Foreign body giant cells (granuloma)

A

-multinucleated cells formed by macrophages
-encapsulate and isolate offending agents

PATHO (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions