Brainscape's Knowledge GenomeTM

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


See full index

Veterinary Pathology > Term Test 2 - Inflammation > Flashcards

Term Test 2 - Inflammation Flashcards

1
Q

what leukocyte is present in most lesions of acute inflammation

A

neutrophils (at least some)

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

pus implies what

A

bacterial infection

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

what are some examples of causes of neutrophilic inflammation

A

trauma, burns, immune complexes, foreign material, thrombosis, necrosis

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

neutrophils enter tissues within _______

A

hours

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

pus takes __________ days to form

A

several

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

abscess has what specific connotations

A

implies fibrosis, which takes at least a week (4-5 days to start)

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

What is the fate of a neutrophil

A

typically death once they enter a tissue

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

What are the four outcomes of suppurative inflammation

A

1) resolution - if the stimulus is removed
2) chronic suppurative inflammation - if stimulus persists
3) stimulation of fibrosis
4) containment - abscess formation

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

Do neutrophilic infections always produce pus

A

NO. If the neutrophils are contained in many compartments (ex. alveoli) or non-liquid, pus will not be produced

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

What are the steps in neutrophil recruitment (8 total)

A

1) bacteria enter tissue
2) bacteria are recognized by antibodies, phagocytes, complement…
3) release of inflammatory mediators
4) inflammatory mediators act on the endothelium and leukocytes
5) rolling adhesion (mediated by selectins)
6) firm adhesion (mediated by integrins)
7) diapedesis
8) chemotaxis

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

What are 3 mediators of chemotaxis

A

IL-8, C5a, LTB4

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

Rolling is mediated by ______ on leukocytes and ___________ on endothelium

A

carbohydrates ; L-selectin/P-selectin

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

Firm adhesion is mediated by ______ on leukocytes and ___________ on endothelium

A

integrins (ex. LFA1 aka CD11a/CD18); ICAM-1

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

How do neutrophils undergo chemotaxis

A

Extension of lamellipodia that adhere to the tissue matrix

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

What is an example of a chemotactic molecule for neutrophils

A

IL-8

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

What is an example of a chemotactic molecule for eosinophils

A

RANTES

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

What is an example of a chemotactic molecule for both neutrophils and eosinophils

A

C5a

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

IgG binds to _________ and is an opsonin of ____________ immunity

A

FcγR; acquired

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

C3b binds to ________ and is an opsonin of ____________ immunity

A

CR3; innate and acquired

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

SP-A and MBL are opsonins of _____________ immunity

A

innate

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

What TLR recognizes bacterial lipoproteins

A

TLR1, 2, 6

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

What TLR recognizes bacterial LPS

A

TLR4

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

What TLR recognizes CpG DNA

A

TLR9

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

What TLR recognizes dsRNA

A

TLR3

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

What TLR recognizes flagellin

A

TLR5

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

What TLR recognizes ssRNA

A

TLR7,8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are 4 mechanisms by which neutrophils kills bacteria

A

bactericidal proteins, oxidative killing, proteolytic enzymes, NETs

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

what are 4 types of antimicrobial proteins in neutrophil granules

A

lactoferrin, lysozyme, defensins, cathelicidins

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

what are 4 types of ROS

A

superoxide anion (O2-), hypochlorite (HOCl-) , peroxide (H2O2), myeloperoxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are 3 types of proteolytic enzymes

A

elastase, collagenase, cathepsin G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How do leukocytes recognize bacteria (3)

A

1) opsonins, 2) PAMPs, 3) cytokines from other cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How do leukocytes kill bacteria (4)

A

1) bactericidal enzymes, 2) oxidative killing, 3) proteolytic enzymes, 4) NETs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the stimulus for eosinophils (2)

A

Parasites and allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are eosinophil effector functions

A

1) not phagocytic
2) oxidative injury
3) damage to cell membranes from granule proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are eosinophil granule proteins (3)

A

Eosinophil myeloperoxidase, eosinophil major basic protein; eosinophil cationic protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

T/F low amounts of immune complexes are characteristic of many immune reactions

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

In what cases do immune complexes cause disease

A

Persistent infection/immune response or defective removal via phagocytosis and complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where do circulating immune complexes tend to deposit

A

synovium, glomeruli, skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is the Arthus reaction

A

when antigen localized to vessel walls reacts with circulating antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is a granuloma

A

nodular mass of activated (epitheloid) macrophages, with or without giant cells, surrounded by lymphocytes and/or fibrous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is granulomatous inflammation

A

inflammation dominated by activated macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

T/F granulomatous inflammation often includes giant cells, epitheloid macrophages and fibrosis

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is pyogranulomatous inflammation

A

Dominated by activated macrophages and neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

T/F granulomatous inflammation can be acute or chronic

A

FALSE, it is ALWAYS CHRONIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are four causes of granulomatous inflammation

A

1) foreign material
2) fungi
3) mycobacterium
4) DTH reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the pathogenesis of granulomatous inflammation

A

Response to inert foreign material OR immune response stimulated by Th1 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are some sequelae of granulomatous inflammation

A

cachexia, space occupying lesion, impingement on a vital structure

48
Q

How do macrophages become activated during granulomatous inflammation

A

Macrophages present antigen to Th1 cells -> Th1 cells produce IFNγ -> IFNγ activates the macrophages

49
Q

What are the effector functions of macrophages

A

Phagocytosis and killing of bacteria

50
Q

How does granulomatous inflammation differ from neutrophilic inflammation

A

In granulomatous, there are resident populations of macrophages that are ready for rapid responses AND there is better coordination between the immuno-inflammatory responses

51
Q

What are some common causes of delayed type hypersensitivity

A

plants, textile fibres, dyes, cleansers, topical medications, shampoos, disinfectants, rubber, latex, plastics, metals

52
Q

What is the time from exposure to the stimulus to onset of immune complex mediated disease

A

8 hours

53
Q

What is the time from exposure to the stimulus to onset of delayed type hypersensitivity

A

24-72 hours

54
Q

How would you describe the exudate formed by neutrophilic inflammation on mucosal surfaces

A

catarrhal or mucopurulent

55
Q

What is hypopyon

A

neutrophilic inflammation in the anterior chamber of the eye; interferes with vision

56
Q

endothelial activation is associated with an _______ in tissue factor _______ in protein C and ________ in thrombomodulin

A

increase, decrease, decrease

57
Q

what colour does eosinophilic inflammation impart on tissues

A

green

58
Q

What are three ways that neutrophils may damage host tissue

A

space occupying lesion, proteolytic/oxidative injury, induction of fibrosis and scarring

59
Q

what are giant cells

A

macrophages with multiple nuclei (5-20)

60
Q

T/F there are tons of lymphocytes in a granulomatous reaction to foreign bodies

A

FALSE

61
Q

What are histiocytes

A

macrophages, monocytes, dendritic cells

62
Q

Inflammatory lesions formed by lymphocytes +/- plasma cells without other leukocytes suggests

A

protozoal, viral, or immune-mediated disease

63
Q

What is SIRS

A

Systemic consequences of localized or disseminated inflammation

64
Q

What is sepsis

A

SIRS caused by infection

65
Q

What is bacteremia

A

Bacteria in systemic circulation (with or without clinical disease)

66
Q

What is septicemia

A

Bacteremia + clinically apparent disease

67
Q

Name examples of systemic distribution of the causes of SIRS

A
  • bacteremia
  • anaphylaxis
68
Q

Name examples of localized distribution of the causes of SIRS

A
  • sterile pancreatitis
  • bacterial pneumonia
69
Q

What are examples of cytoplasmic receptors

A

NOD like receptors and RIG-I like receptors

70
Q

What are three examples of soluble receptors

A

complement, antibody, collectins

71
Q

What are examples of cell surface receptors

A

TLRs, Fc receptors, complement receptors

72
Q

Changes in tissue factor, thrombomodulin and protein c promote _____________ when local

A

endothelial activation and hypercoagulability -> thrombosis

73
Q

Changes in tissue factor, thrombomodulin and protein c promote __________ when disseminated

A

cogaulation -> DIC -> consumptive coagulοpathy

74
Q

Name 5 consequences of SIRS

A
  1. acute phase response
  2. vasodilation (systemic hypotension)
  3. increased vascular permeability (edema)
  4. leukocyte activation (release of proteases and free radicals)
  5. endothelial activation
75
Q

What tissues are the first to suffer from SIRS

A

liver, heart, brain, kidney, intestine, lung

76
Q

T/F acute phase response is static

A

False, it is adaptive

77
Q

Define the acute phase response

A

systemic changes in physiologic processes during disease; adaptive

78
Q

Name 3 acute phase proteins

A

CRP, fibrinogen, haptoglobin

79
Q

Name 3 beneficial functions of acute phase proteins

A

control pathogens, quell inflammation, minimize tissue damage

80
Q

Name 2 acute phase proteins in ruminants

A

haptoglobin, fibrinogen

81
Q

Name 2 acute phase proteins in dogs

A

SAA, CRP

82
Q

Name 2 acute phase proteins in cats

A

SAA, α1 acid glycoprotein

83
Q

Which is most likely to trigger an acute phase response
A) bacterial pneumonia
B) dehiscence of GI tract
C) liver abscess
D) granuloma in cat liver

A

B (tons of bacteria, huge surface area affected)

84
Q

Where is edema commonly localized to during SIRS

A

lung

85
Q

Define autoimmune disease; what breaks down

A

Disease caused by an immune response against self-antigens (Ab mediated and cell mediated); breakdown of self tolerance

86
Q

Name three mechanisms of tissue damage in autoimmune diseases and give an example of each

A

1) immune complex disease (vasculitis, polyarthritis, glomerulonephritis, uveitis)
2) antibody-mediated cytotoxicity (IMHA, thrombocytopenia, myasthenia gravis, pemphigus)
3) T cell-mediated cytotoxicity (myositis, discoid lupus)

87
Q

What is inflammation

A

The active response of tissues to injury which stimulates a return to homeostasis

88
Q

Neutrophils eliminate

A

extracellular bacteria

89
Q

Eosinophils eliminate

A

metazoan parasites (worms)

90
Q

Macrophages eliminate

A

Mycobacteria, fungi, foreign material

91
Q

Cytotoxic T cells eliminate

A

viruses, protozoa

92
Q

Name 4 goals of inflammation

A

1) eliminate the injurious stimulus or pathogen
2) contain the injury
3) remove necrotic tissue
4) initiate tissue repair

93
Q

Humoral responses of inflammation include (5)

A

Fibrinogen, edema, antibody, innate defense proteins, complement

94
Q

What occurs physiologically during cachexia and why

A

Catabolism of muscle to provide amino acids for tissue repair

95
Q

The plasma concentration of acute phase protein increases within _____________ hours after the onset of tissue injury

A

5-10

96
Q

The plasma concentration of acute phase proteins returns to normal within by _________ hours after the inflammatory response subsides

A

48 (2 days)

97
Q

Measuring the concentration of _____________ is helpful to detect inflammatory responses in ruminants

A

plasma haptoglobin

98
Q

What are the most frequent sites for bacteremic spread

A

pericardium, pleura, peritoneum, meninges, synovial surfaces

99
Q

What well vascularized tissues are prone to population from bacteria

A

Cancellous bone, growth plate of bones, spleen, liver, kidney, lung, uvea, heart valves

100
Q

What is a consequence of hypercoagulability in horses

A

laminitis

101
Q

What are four ways in which autoimmune diseases damage tissues

A

1) antibody mediated opsonization/complement activation
2) formation of immune complexes
3) pro inflammatory/cytotoxic effects of autoreactive T cells
4) actions of T helper cells

102
Q

What three changes indicate that an inflammatory reaction is occuring in a patient

A

1) fever
2) leukocytosis
3) changes in acute phase proteins

103
Q

What are the three MAIN organs that get affected during SIRS/sepsis

A

kidney, liver, lung

104
Q

T/F neutrophils secrete cytokines that can trigger thrombosis, leading to ischemia

A

T

105
Q

what is activated upon immune complex deposition

A
  1. activation of complement
  2. activation of macrophages and neutrophils
106
Q

what causes vasculitis

A

neutrophil-mediated damage to vessel walls (by being recruited to the vessel wall)

107
Q

T/F well vascularized tissues are the most susceptible to immune complex disease

A

T

108
Q

What are two consequences of immune complex deposition

A
  1. vasculitis (due to the neutrophils)
  2. activation of platelets and thrombosis -> infarction and ischemia
109
Q

T/F Mycobacterium = mycoplasma

A

F

110
Q

T/F macrophages activated by IFNγ are better equipped at killing intracellular pathogens

A

T

111
Q

upon re-exposure to an antigen that elicited a TH1 response, what happens

A

TH1 cells secrete cytokines that induce an inflammatory response and IFNγ that activates macrophages

112
Q

Type 1 sensitivity takes how many mins to develop

A

30

113
Q

Type III sensitivity takes how long to develop

A

8 hours

114
Q

Type IV sensitivity takes how long to develop

A

24-72h

115
Q

what are three consequences of vasculitis from immune complex deposition

A

edema, petechiae, infarcts

116
Q

How does the histologic appearance of a chronic allergic disease differ from that of the immediate reaction following injection of an allergen?

A

chronic: mast cells, eosinophils, lymphocytes

acute: degranulated mast cells, edema

117
Q

In pemphigus foliaceus, how does the immune response cause pustules/ vesicles/ blisters in the epidermis?

A

Autoantibodies target desmosomal proteins

Veterinary Pathology (7 decks)

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