Brainscape's Knowledge GenomeTM

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


See full index

COM - MOD 1 > Ch 3 - 5/6 Dobson > Flashcards

Ch 3 - 5/6 Dobson Flashcards

1
Q

Asthma is due to what cells?

A

Eosinophils, IgE Abs

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

Glomerulonephritis is due to what cells?

Acute or chronic?

A

Abs and complement, neutrophils, monocytes

Acute

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

Septic shock is due to what cells?

Acute or chronic?

A

Cytokines

Acute

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

Arthritis is due to what cells?

Acute or chronic?

A

Lymphocytes, macrophages

Chronic

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

Atherosclerosis is due to what cells?

Acute or chronic?

A

Macrophages, lymphocytes

Chronic

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

Pulmonary fibrosis is due to what cells?

Acute or chronic?

A

Macrophages, fibroblasts

Chronic

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

What kind of inflammation is characterized by the following: mostly neutrophils, prominent local and systemic signs, mild and self-limited tissue injury, fibrosis

A

Acute inflammation

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

Primary granules (azuorphilic) contain what?

How are they described?

A

NADPH oxidase, MPO, lysosomal enzymes

Larger

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

Secondary (specific) granules contain what?

Described as what?

A

Lysozyme, collagenase, gelatinase, lactoferrin, histaminase

Smaller

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

What is the source of histamine?

Action?

A

Mast cells, basophils, platelets

Vasodilation, INC vascular permeability, endothelial activation

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

What is the source of PGs?

Action?

A

Mast cells, leukocytes

Vasodilation, pain fever

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

What is the source of LTs?

Action?

A

Mast cells, leukocytes

Inc vascular permeability, chemotaxis, leukocyte adhesion and activation

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

What is the source of cytokines?

Action?

A

Macrophages, endothelial cells

Local: endothelial activation
Systemic: fever, metabolic abnormalities, hypotension (shock)

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

What is the source of PAF?

Action?

A

Leukocytes, mast cells

Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, oxidative burst, de granulation

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

What is the source of complement?

Action?

A

Plasma (made in liver)

Leukocyte chemotaxis and activation, vasodilation, direct target killing

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

What is the source of kinins?

Action?

A

Plasma (made in liver)

INC vascular permeability, smooth muscle contraction, vasodilation, pain

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

What PGs or LTs are responsible for vasodilation?

A

PGI2, PGE1, PGE2, PGD2

DIEE12

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

What PGs or LTs are responsible for vasoconstriction?

A

TxA2, LTC4, LTD4, LTE4

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

What PGs or LTs are responsible for increased vascular permeability?

A

LTC4, LTD4, LTE4

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

What PGs or LTs are responsible for chemotaxis and leukocyte adhesion?

A

LTB4, HETE

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

What PGs or LTs are responsible for bronchospasm?

A

LTC4, LTD4, LTE4

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

What do steroids inhibit?

A

Phospholipases

Therefore the entire PG/LT pathway

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

What is an inhibitor of inflammation?

What enzyme makes these?

A

LXA4 and LXB4

12-LO

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

What are the key mediators of chronic inflammation?

A

IL-12
IFN-gamma
IL-17

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

What is the source of IL-12?

Action in inflammation?

A

DC, macrophages

INC production of IFN-gamma

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

What is the source of IFN-gamma?

Action in inflammation?

A

T lymphocytes, NK cells

Activation of macrophages

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

What is the source of IL-17?

Action in inflammation?

A

T lymphocytes

Recruitment of neutrophils and monocytes

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

What is the source of TNF?

Action in inflammation?

A

Macrophages, mast cells, T lymphocytes

Stimulates expression of endothelial adhesion molecules and secretion of other cytokines

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

What is the source of IL-1?

Action in inflammation?

A

Macrophages, endothelial cells

similar to TNF
Important in Fever

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

What is the source of IL-6?

Action in inflammation?

A

Macrophages

Acute phase response

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

Complement system is a collection of what kind of proteins?

A

Soluble

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

What are the actions of bradykinin?

A

INC vascular permeability
Causes contraction of smooth muscle
Dilation of blood vessels
Pain when injected into skin

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

Serous inflammation is most commonly seen in what body cavities?

A

Peritoneum, pleura, pericardium

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

Suppurative or liquefactive necrosis indicates what kind of infection?

A

Bacterial infection

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

Chronic inflammation causes include persistent infection, what are some of the most common?

A

Myobacteria
Virus
Fungi
Parasites

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

What kind of cells typify chronic inflammation?

A

Macrophages
Lymphocytes
Plasma cells

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

What activates M1 macrophages?

A

Microbes, IFN-gamma

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

M1 Macrophages secrete what cytokines that will increase inflammation?

A

IL-1, IL-12, IL-23

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

M1 macrophages can perform phagocytosis, via what mediators?

A

ROS, NO, lysosomal enzymes

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

What activates M2 Macrophages?

A

IL-4, IL-13

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

M2 macrophages secrete what cytokines for tissue repair and fibrosis?

Anti-inflammatory effects?

A

GFs, TGF-B

IL-10, TGF-B

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

What type of CD4 cells is responsible for defense against extracellular bacteria and fungi?

Secretes what cytokines?

A

TH17

IL-17, IL-22

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

Granulomatous inflammation is a form of chronic inflammation characterized by what type of cells?

Sometimes associated with what?

A

Activated macrophages and T lymphocytes

Central necrosis

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

What are the systemic effects of inflammation?

A

Fever
Acute-phase reactants
Leukocytosis

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

What are the 4 clinically important acute-phase reactants?

A

CRP
Fibrinogen
SAA
Hepcidin

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

Elevated CRP indicates what?

A

risk for MI

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

Fibrinogen is measured how?

A

ESR, rouleaux formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Hepcidin is measured for what?

A

Anemia of chronic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Bacterial infections are characterized by what cells usually?

Viral?

A

Neutrophils

Lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Decreased white cells is called what?

A

Leukopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Allergies and parasite infections are characterized by what?

A

Eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is a left shift?

A

Putting out increased numbers of immature forms of neutrophils in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are organs/locations where you do not what fibrosis?

A 
Eye
Lung
GI
Heart
Skin
Liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Acute respiratory distress syndrome is due to what cells?

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Who said that inflammation is not a disease, but a stereotypic response?

A

John Hunter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Who established the concept that chemical substances like histamine mediate vascular change in inflammation?

A

Sir Thomas Lewis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Who discovered phagocytosis via observation of amebocytes?

A

Ellie Metchnikoff

58
Q

What mediators are responsible for the immediate transient response?

A

Histamine, bradykinin, LTs

59
Q

What stimulates transcytosis?

What else does it do?

A

VEGF

Promotes vascular leakage

60
Q

What is the mainly responsible for a creating transudates fluid?

A

Decreased colloid osmotic pressure (liver disease) or increased protein loss (kidney disease)

61
Q

During leukocyte rolling, what is expressed on the endothelium to slow down leukocytes?

On the leukocytes themselves?

A

P-selectin (from Weibel-Palade) bodes and E-selectin

L-selectin and ligands for P and E selectin

62
Q

What do selectins bind on leukocytes?

A

Sialyl Lewis X bodies

63
Q

During adhesion, what induces expression of Integrins on leukocytes?

What specific Integrins?

A

TNF and IL-1

VCAM-1 and ICAM-1

64
Q

Leukocyte migration is via what?

Where does it occur?

What is involved?

A

Transmigration/diapedesis

Postcapillary venules

CD-31/PECAM-1

65
Q

What is mainly responsible for chemotaxi of leukocytes?

A

IL-8, C5a, LTB4

66
Q

What kind of infection is dominated by neutrophils for several days as opposed to macrophages?

A

Pseudomonas bacteria

67
Q

What are the most common exogenous agents?

A

Bacterial products containing N-fMet

68
Q

What is the ligand for ICAM-1, located on monocytes and DCs?

On neutrophils?

A

MAC-1

LFA-1

69
Q

What are the ligands for VCAM-1, located on T cells?

A

VLA-4

Alpha4-Beta7

70
Q

What is responsible for leukocyte activation?

A

Increased cytosolic Ca and activation of PKC and PLA2

71
Q

What are the major opsonins?

72
Q

What is the phagocytosis dependent on?

A

Polymerization of actin filaments

73
Q

Oxygen to superoxide anion is done by what enzyme?

Reduction or oxidation?

Happens where most often? Accompanies what?
Called what specifically?

A

NADPH oxidase

Reduction

Neutrophils
Phagocytosis
Respiratory Burst

74
Q

Superoxide anion to hydrogen peroxide by what enzyme?

75
Q

Where are ROS produced?

A

Within the lysosome and phagolysosome

76
Q

Hydrogen peroxide to hypochlorite (HOCl/OCl2) via what?

Happens where?

A

MPO

Azuorphilic granules of neutrophils

77
Q

When is iNOS induced?

What does it catalyze?

A

When macrophages and neutrophils are activated by IFN-gamma or microbial products

Arg –> NO

78
Q

What can cleave C3 and C5 yielding anaphylatoxins?

A

Neutral proteases

79
Q

What is the major inhibitor of neutrophil elastase?

A

Alpha1-antitrypsin

80
Q

What is in small (secondary) neutrophil granules?

A

HAP to LowerLevel Grand Central

Histaminase
Alkaline phosphatase
Plasminogen activator

Lactoferrin
Lysozyme

Gelatinase
Collagenase

81
Q

What is in larger primary neutrophil granules?

A

MPO

Acid hydrolases

82
Q

What is lactoferrin?

A

Iron-binding protein

83
Q

What is major basic protein?

A

Cationic protein of eosinophils, cytotoxic to parasites

84
Q

NET formation leads to what?

A

Loss of nuclei, death of the cell

85
Q

What is stored in preformed molecules and are released 1st during inflammation?

A

Histamine and serotonin

86
Q

What do eicosanoids do?

A

Mediate inflammation and bind GPCRs

87
Q

What activates acute phase proteins from the liver?

88
Q

What stimulates leukocyte production from the bone marrow?

A

TNF
IL-1
IL-6

89
Q

What are C-C chemokines that attract monocytes, eosinophils, basophils, lymphocytes?

A

MCP-1
Eotaxin
MIP-1a
RANTES

90
Q

What is the only CX3C chemokines?

What forms?

A

Fractalkine

Cell-surface bound and soluble form with chemoattractant activity

91
Q

What is responsible for inhibiting viral replication?

A

Type I IFN

92
Q

Inherited deficiency of this factor leads to hereditary angioedema?

A

C1 inhibitor

93
Q

What blocks formation of C3 convertase?

94
Q

What inhibits MAC formation?

95
Q

What does PAF cause?

At low []’s what does it do?

Associated with what?

A

Platelet aggregation, vasoconstriction, bronchoconstriction

Induces vasodilation and increased vascular permeability

ADP

96
Q

What is an effusion?

A

Fluid from plasma or secretions of mesothelial cells

97
Q

Serous inflammation is marked by what?

What linings of the body?

Example?

A

Exudation of cell-poor fluid into spaces created by cell injury into body cavities lined by

Peritoneum, pleura, pericardium

Skin blistering after burn, viral infection

98
Q

When does a fibrinous exudate develop?

Characteristic of what body cavity linings?

A

When vascular leaks are large or there is a local Procoagulant stimulus (cancer cells)

Meninges, pericardium, pleura

99
Q

What bacterial infection is most common in purulent inflammation?

Example?

A

Staphylococci

Appendicitis

100
Q

What are localized collections of purulent inflammatory tissue?

Produced by what?

A

Abscesses

Seeding of pyogenic bacteria into a tissue

101
Q

What is a local defect, excavation of the surface of an organ or tissue that is produced by the sloughing of inflamed necrotic tissue?

102
Q

What is the most common locations of ulcers?

A

Mucosa of the mouth, stomach, intestine, genitourinary tract AND

Skin and subcutaneous tissue of the lower extremities in older people

103
Q

When does chronic inflammation occur?

A

Persistent infection
Hypersensitivity disease
Prolonged exposure to toxic agent

104
Q

What is chronic inflammation characterized by?

A

Infiltration of macrophages, lymphocytes, plasma cells
Tissue destruction
Attempts at healing

105
Q

Macrophages in the spleen and LNs are called what?

A

Sinus Histiocytes

106
Q

In what condition of chronic inflammation may neutrophils be present and dominate?

A

Osteomyelitis

107
Q

What comes together to form tertiary lymphoid organs in some chronic inflammatory reactions?

Examples?

A

Lymphocytes, APCs, plasma cells

R.A. And Hashimoto’s

108
Q

How do you identify a foreign body Granuloma?

Examples?

A

Center of Granuloma with polarized light, appears refractile

Talc, sutures

109
Q

In immune granulomas, what do macrophages activate?

A

T cells to produce IL-2 and IFN-gamma

110
Q

Activated macrophages in granulomas have what features?

A

Pink granular cytoplasm with indistinct cell boundaries called epitheloid cells

111
Q

What are sometimes found in granulomas?

A

Langhans giant cells

112
Q

In what disease/condition is there non-caseating necrosis present with granulomas?

A

Crohn’s
Sarcoidosis
Foreign body reaction

113
Q

What kind of tissue reaction does Myobacterium leprae cause?

A

Acid-fast bacilli in macrophages

Noncaseating Granuloma

114
Q

What type of tissue reaction does Treponema pallidum cause?

What disease?

A

Gemma, plasma cell inflitrate, no loss of cellular outline

Syphillis

115
Q

What causes cat-scratch disease?

Tissue reaction?

A

Gram-negative bacillus

Rounded or stellate Granuloma, giant cells UNCOMMON

116
Q

Describe the formation of Granuloma starting with macrophages and ending with epitheloid cells:

A

Macrophages secrete IL-12 -> Th1 -> IFN-gamma -> epitheloid cells

117
Q

What are the clinical manifestations of the acute phase response?

A 
INC BP and pulse
DEC sweating 
Shivering
Chills
Anorexia
Malaise
118
Q

Typhoid fever, rickets, or Protozoa results in what condition?

A

Leukopenia

119
Q

Erythrocyte sedimentation rate (ESR) is used to look for rouleaux formation to test for what?

A

Fibrinogen

120
Q

What is used as a marker for increased risk of MI in patients with CAD?

A

Elevated serum CRP

121
Q

What acute-phase reactant has implications in anemia when present in increased [ ]’s?

122
Q

What are Labile tissues?

Examples

A

Continuously dividing

HSC in bone marrow, surface epithelium of skin, oral cavity, vagina, cervix, gi, uterus urinary tract

123
Q

Describe stable tissues

Examples?

A

Minimally proliferative activity in normal state, quiescent (G0)

Parenchymal of liver, kidney, pancreas
Endothelial cells, fibroblasts, smooth m. Cells

124
Q

What are the types of permanent tissue?

A

Cardiac
Neuronal
Skeletal muscle

125
Q

Where do progenitor cells of the liver reside?

A

Canals of Hering

126
Q

What mediator is responsible for the priming phase of liver regeneration?

Growth factor phase?

Termination phase?

A

IL-6

HGF and TGF-a

TGF-B

127
Q

The sprouting of new blood vessels due in the inflammation/angiogenesis stage of scar formation is due to what?

What stimulates the proliferation of endothelial cells and the migration of macrophages and fibroblasts to the damaged area?

A

VEGF-A

FGF-2

128
Q

What GFs play a role in structural maturation of new vessels and angiogenesis?

A

Ang1 and Ang2

129
Q

What is the receptor for Ang1?

130
Q

What GF regulates sprouting and branching of new vessels via cross talk with VEGF?

131
Q

What GF participates in the process of vessel sprouting via interactions with integrin receptors by providing scaffold for vessel growth?

A

ECM proteins

132
Q

What enzymes in the ECM degrade the ECM to permit remodeling and extension of the vascular tube?

A

Matrix metalloproteases (MMPs)

133
Q

What regulates the deposition of CT in scar formation?

Activated by what?

A

PDGF, FGF-2, TGF-B

M2 macrophages

134
Q

What cells contribute to contraction of the scar over time?

A

Myofibroblasts

135
Q

In the remodeling of CT, what degrades collagens? What are they dependent upon?

What inhibits them to shut down activity?

A

MMPs, metal ions (zinc)

TIMPs

136
Q

What is anchored to the PM and cleaves and releases extracellular domains of cell-associated cytokines and GFs like TNF, TGF-B?

137
Q

If the injury involves only the epithelial layer, how does wound healing progress?

Example?

A

Primary intention

Sutures

138
Q

When cell loss is extensive, as in large wounds, abscesses, ulceration, and ischemic necrosis, how does healing occur?

A

Secondary intention

139
Q

An accumulation of excessive amounts of collagen creating a raised scar is called what?

A

Hypertrophic scar

140
Q

Scar that grows beyond the boundaries of the original wound but does not regress is called what?

Common in what population?

Characterized by what?

Common in what part of the body?

A

Keloid

African Americans

Type 3 collagen

Earlobe, face, upper extremities

141
Q

Where are contractures prone to develop?

Commonly seen when?

A

Palms, soles, anterior thorax

After burns and compromise the movement of joints

COM - MOD 1 (7 decks)

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