ACVS > Chapter 1 - Inflammatory Response > Flashcards

Chapter 1 - Inflammatory Response Flashcards

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1
Q

What cells produce TNF-α?

A

Activated M1 macrophages are a major source of TNF-alpha.

Also made by:Monocytes, macrophages, neutrophils, NK cells, and several others (T, B, fibroblasts).

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2
Q

What is stimulated by the release of TNF-α?

A

Production of proinflammatory cytokines (e.g., IL-6), reactive oxygen intermediates, chemotaxins, and endothelial adhesion molecules (all facilitate the recruitment of cells at the site of inflammation).

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3
Q

The main effect of TNF-α is stimulation of cytokines (IL-6, ROS, etc.) that facilitate cell recruitment at the site of inflammation. What are three additional effects of TNF-α?

A

Activation of natural killer cells, proliferation of cytotoxic T-cells, and T-cell apoptosis.

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4
Q

What are released from the cell surface to reduce the activity of TNF-α?

A

Tumor necrosis factor soluble receptors

Found constitutively at low levels in the blood but are increased in inflammatory conditions such as sepsis. The solubilized receptors bind to TNF-α and effectively reduce the cytokine’s activity.

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4
Q

TNF-α has both beneficial and deleterious effects. Name some of each:

A

Beneficial - protects against mycobacterial infection, blocking it in septic patients increases mortality

Deleterious - causes all the classic signs of shock (hypotension, metabolic acidosis), causes inflammation (inflammatory diseases like Crohns).

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5
Q

What is TNF-α?

A

A membrane-bound surface protein, cleaved by metalloproteases, that is released in soluble form.

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6
Q

Corticosteroids and recombinant TNFR receptors (Enbrel, a treatment for RA/Crohn’s) inhibit TNF-α, which increases risk of what?

A

Recrudescence of pulmonary mycobacterial infections and infectious complications after orthopedic surgeries.

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7
Q

True or False: Activated M1 macrophages produce proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and prostaglandins, enhancing the inflammatory response?

A

True

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8
Q

True or False: M2 macrophages are activated in response to proinflammatory cytokines?

A

False. M2 macrophages are activated in response to anti-inflammatory cytokines (IL-4, IL-13, and IL-10). They then secrete growth factors like PDGF or TGF-β, which stimulate fibroblasts to produce collagen, aiding in wound healing and further dampening the inflammatory response.

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9
Q

True or False: M1 macrophages are activated by infectious agents or proinflammatory cytokines?

A

True. M1 macrophages are activated by infectious agents or proinflammatory cytokines (interferon-gamma [IFN-γ] or TNF-α). They then produce more proinflammatory cytokines and prostaglandins to increase inflammation.

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10
Q

As the acute inflammatory response resolves, macrophages produce factors that stimulate fibroblasts to produce ________, aiding in wound repair and healing of the inflamed tissue?

A

Collagen! Fibroblasts are the most common cell that produce collagen.

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11
Q

Prostaglandins are produced in the __________ pathway?

A

Prostaglandins are produced in the cyclooxygenase (COX) pathway.

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12
Q

What is the starting molecule for prostaglandins?

A

Arachidonic acid (metabolized along the cyclooxygenase pathway containing COX enzymes).

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13
Q

COX-2 expression is induced by what?

A

Trauma, growth factors, proinflammatory cytokines, and other mediators.

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14
Q

True or False: COX-1 is constitutively expressed (always present)?

A

True. It is involved in homeostasis and is present in the majority of mature cells.

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15
Q

What is the precursor to all prostaglandins and thromboxanes?

A

PGH2 (Prostaglandin H2).

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16
Q

Describe the arachidonic acid pathway?

A

AA -> through COX -> PGG2 -> releases free oxygen radicals to become -> PGH2 -> ENZYMES = Thromboxane A2 and B2, PGE2, PGF2, and PGI2 (prostacyclin).

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17
Q

How long do macrophages live in circulation vs. in tissues?

A

Circulation: days
Tissues: Months to years

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18
Q

Pattern-recognition receptors (PRRs) are promiscuous, what does that mean, baby?

A

They can bind to multiple alarm signal molecules -> inflammation

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19
Q

What are Toll-Like receptors (TLRs) important for?

A

They play a central role in the release of pro-inflammatory cytokines from the innate immune system in response to microbial structures (they recognize bacteria)

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20
Q

What cells contain histamine?
What is the major histamine receptor in inflammation?
When is the peak response to histamine seen?

A

Mast cells (but also platelets and basophils)

H1 receptor on endothelial cells -> arteriolar vasodilation/venule permeability but large artery vasoconstriction

Short half life, peak response is 15-20 min

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21
Q

On initial injury, what (4) things cause vasodilation/inflammation?

A

Catecholamines
Serotonin
Prostaglandins
Bradykinin

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22
Q

Within minutes, what (5) things are in control of inflammation?

A

Nitric oxide
histamine
leukotrienes
Prostaglandins
Complement

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23
Q

What are the first migratory cells to arrive? When do they peak?

A

Neutrophils
Peak at 24-48hr

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24
What are the proinflammatory cytokines?
TNF-a IL-1B IL-6 IL-8
25
What are the two main anti-inflammatory cytokines?
IL-1ra IL-10
26
IL-6 plays a pivotal role in what process?
Hepatic production of acute phase proteins
27
IL-10 limits inflammatory reaction to what normal body thing?
Gut bacteria
28
Negative acute phase proteins decrease by what % in inflammation? What is the major negative acute protein?
25% Albumin
29
Positive acute phase proteins increase by at least 25% in inflammation. What are (3) main ones?
C-reactive protein Serum amyloid A Serum amyloid P
30
Microbe detection / activation of the complement pathway causes three responses - what are they?
Inflammation Phagocytosis Membrane attack complex formation to lyse a microbe directly
31
Which five cardinal clinical signs define acute inflammation, and what is the fifth functional consequence often listed after the classic four?
Rubor (redness), calor (heat), dolor (pain), tumor (swelling), and loss of function (functio laesa).
32
Immediately after tissue injury, what is the typical arteriolar response and what is its primary purpose?
A rapid, transient arteriolar vasoconstriction occurs, primarily to promote hemostasis.
33
Which mediators are listed as contributors to the early, transient vasoconstriction that follows acute injury?
Catecholamines, serotonin, prostaglandins, and bradykinin from local tissues, plus norepinephrine from the sympathetic nervous system.
34
Within minutes after injury, what arteriolar change predominates and what is the physiologic goal of that change?
Vasodilation predominates to increase blood flow and deliver inflammatory cells and soluble mediators.
35
Which mediators are listed as major drivers of early vasodilation in acute inflammation?
Nitric oxide (NO), histamine, leukotrienes, prostaglandins, and complement.
36
In acute inflammation, increased vascular permeability in venules is largely mediated by what structural endothelial change and which mediators trigger it?
An increased number and size of endothelial gaps in venules, triggered by histamine and serotonin.
37
What is transcytosis during inflammation and what does it allow to reach the inflamed site?
Transport of plasma products across endothelial cells, allowing plasma proteins and other soluble mediators to enter inflamed tissues.
38
How does increased vascular permeability contribute to edema and leukocyte delivery at the inflamed site?
Protein-rich fluid loss lowers intravascular oncotic pressure and increases viscosity, promoting edema and slowing flow so leukocytes can marginate and extravasate.
39
What is 'stasis' during acute inflammation and how does it promote leukocyte extravasation?
Fluid loss causes hemoconcentration and congestion, producing intravascular stasis; slower flow increases leukocyte-endothelium contact time, promoting margination and extravasation.
40
Which adhesion molecules primarily mediate leukocyte margination and rolling during extravasation?
Endothelial selectins interacting with leukocyte ligands.
41
Which cytokine class stimulates leukocyte integrin expression and affinity changes needed for firm adhesion?
Chemokines.
42
Firm leukocyte adherence to endothelium is mediated by leukocyte integrins binding to which endothelial ligand example provided?
Endothelial cell integrins/adhesion molecules such as ICAM-1.
43
Leukocyte diapedesis is facilitated by which platelet–endothelial adhesion molecule?
PECAM-1 (platelet–endothelial cell adhesion molecule).
44
After diapedesis, how do leukocytes localize to the injury site?
They follow chemokine concentration gradients (chemotaxis).
45
In acute inflammation, which leukocyte is the primary early participant and when does it typically peak in tissues?
Neutrophils; they are the first migratory cells and typically peak at 24–48 hours.
46
Name three major antimicrobial/effector functions of neutrophils listed in the chapter notes.
Phagocytosis, superoxide radical (oxidative burst) release, and formation of extracellular traps (NETs).
47
Which contents characterize neutrophil azurophilic (primary) granules?
Myeloperoxidase, defensins, lysosomal hydrolases, and neutral proteases.
48
Which contents characterize neutrophil secondary granules in the notes?
Metalloproteases.
49
What is emphasized as a key feature of neutrophil gelatinase (tertiary) granules?
They contain preformed receptors that enhance cellular communication and are mobilized to increase surface receptor availability.
50
During early inflammation, what two-stage process occurs in circulating neutrophils and what is the immediate granule-related event?
A rapid priming process occurs; tertiary granules mobilize to increase cell-surface receptors, with additional de novo receptor and cytokine expression induced.
51
How are neutrophils typically cleared from tissues and what anti-inflammatory consequence is noted during their clearance?
They undergo necrosis/apoptosis or are sloughed; when cleared by macrophages, anti-inflammatory mediators are released.
52
In sepsis, what change in neutrophil apoptosis is described and what is the consequence?
Neutrophil apoptosis is delayed, prolonging the proinflammatory state.
53
Which cells are described as tissue-resident 'sentinel' cells responsible for early recognition of inflammatory stimuli?
Tissue-resident macrophages.
54
What is the major early cytokine contribution of tissue-resident macrophages during inflammation?
They are a major early source of pro-inflammatory cytokines.
55
How do circulating monocytes contribute to tissue inflammation according to the notes?
They extravasate in response to chemotaxins and differentiate into macrophages in tissues, becoming a main macrophage population in inflammatory conditions.
56
What is the functional distinction between M1 and M2 macrophage polarization as described?
M1 macrophages are proinflammatory and microbicidal (phagocytosis; IL-1β, IL-6, TNF-α, prostaglandins), whereas M2 macrophages are anti-inflammatory/pro-repair (stimulate fibroblasts and collagen via growth factors).
57
Which cytokines activate M1 polarization in the notes?
Infectious agents or pro-inflammatory cytokines (notably listed as infectious agents or pro-inflammatory cytokines).
58
Which cytokines are listed as promoting M2 macrophage polarization?
IL-4, IL-13, and IL-10.
59
What is the stated timescale for macrophage survival in circulation versus tissues?
Days in circulation; months to years in tissues.
60
Beyond innate immunity, what adaptive immune function of macrophages is explicitly noted?
They function as antigen-presenting cells.
61
Which T-cell subsets are named as major components of cell-mediated immunity?
CD4+ helper T cells and CD8+ cytotoxic T cells.
62
What is the main functional role of Th1 cells in the notes?
They maximize macrophage bacterial killing and stimulate proliferation of cytotoxic T cells.
63
What is the main functional role of Th2 cells in the notes?
They act primarily against helminths and mediate allergic reactions.
64
What triggers mast cell degranulation in acute inflammation according to the notes?
Trauma, complement, microbes, and neuropeptides.
65
Which mediator is identified as the primary source of histamine during acute inflammation, and what other mediators are co-released?
Mast cells; they also release serotonin, leukotrienes, prostaglandins, heparin, and cytokines.
66
During inflammation, what dual role of endothelial cells is highlighted beyond lining vessels?
They can act as antigen-presenting cells and actively regulate permeability, leukocyte extravasation, and coagulation.
67
Which stimuli are noted to activate endothelial cells to rapidly upregulate preformed von Willebrand factor (vWF) and P-selectin?
IL-1β, TNF-β, and bacterial products.
68
After rapid upregulation of preformed molecules, what broader endothelial gene expression changes are described?
De novo expression of proinflammatory cytokines, chemoattractants, and adhesion molecules to promote leukocyte extravasation.
69
What are 'alarm signals' in inflammation and what two broad categories are listed?
Warning molecules that trigger intracellular signaling cascades: pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs).
70
Give three examples of PAMPs listed in the notes.
Lipopolysaccharide (LPS), peptidoglycan, lipoteichoic acid, and microbial oligonucleotides (any three).
71
Give two examples of DAMPs listed in the notes.
Fibrinogen and heat shock proteins.
72
What key property of pattern recognition receptors (PRRs) is emphasized in the notes?
They are promiscuous—each receptor can bind multiple alarm signals—enabling a robust, diverse response.
73
Where can pattern recognition receptors be located according to the notes?
On the cell surface, intracellularly, or as soluble receptors in body fluids.
74
Which PRR family is identified as the most important and what is their core functional outcome?
Toll-like receptors (TLRs); they initiate intracellular signaling cascades that alter gene transcription and drive cytokine release in response to microbial structures.
75
In acute inflammation, where is histamine primarily stored and what makes it an early mediator?
Preformed in granules—primarily mast cells near vessels, also platelets and basophils—so it can be released immediately after injury.
76
Which stimuli are listed as triggers for histamine release?
Physical injury, antibody binding (allergy), complement protein binding, and neuropeptides.
77
What are the primary endothelial effects of histamine via H1 receptors as listed?
Arteriolar vasodilation, increased venular permeability, and constriction of large arteries.
78
What timing feature of histamine action is emphasized in the notes?
Rapid onset with a short half-life; peaks at ~15–20 minutes.
79
How is serotonin characterized relative to histamine in acute inflammation?
It has similar actions but is not a major mediator in acute inflammation.
80
Which four proinflammatory cytokines are highlighted as key in the notes?
TNF-α, IL-1, IL-6, and IL-8.
81
Which cells are identified as major producers of TNF-α in the notes?
M1 macrophages and other activated cell types.
82
Which systemic syndrome signs are attributed to TNF-α in sepsis, and what protective role is also noted?
Hypotension, metabolic acidosis, and death can occur; TNF-α is also necessary for protection from mycobacteria.
83
Which drug class is noted to inhibit TNF-α?
Steroids.
84
How is IL-1 described in terms of activation state and processing?
It is secreted in an inactive form and must be cleaved to an active form.
85
Which cell types are listed as sources of IL-6 and what major systemic function does IL-6 initiate?
Macrophages, T cells, epithelial cells, and enterocytes; IL-6 initiates hepatic production of acute phase proteins.
86
What paradoxical role of IL-6 is noted?
It can also initiate compensatory anti-inflammatory responses.
87
What is IL-8 also called in the notes and what is its principal chemotactic target?
CXCL8; it is a neutrophil chemoattractant.
88
Which two anti-inflammatory cytokines are emphasized in the notes?
IL-1 receptor antagonist (IL-1ra) and IL-10.
89
Which cells are listed as primary sources of IL-10?
CD4+ Th2 cells, monocytes, and B cells.
90
List two anti-inflammatory actions of IL-10 described in the notes.
It depresses production of proinflammatory cytokines/chemokines and promotes shedding of TNF receptors into systemic circulation; it also limits reactions to normal gut-associated bacteria.
91
How do IL-10 levels typically change over time in a balanced immune response, according to the notes?
They are low initially and increase over time.
92
Arachidonic acid (AA) is metabolized through which two major enzymatic pathways to generate inflammatory lipid mediators?
Cyclooxygenase (COX) and lipoxygenase (LOX) pathways.
93
Which pathway produces prostaglandins, and what two classic inflammatory symptoms are prostaglandins linked to in the notes?
COX pathway; prostaglandins contribute to pain and fever and promote vasodilation and leukocyte recruitment.
94
Which COX isoform is described as constitutively present in most cells, and which is inducible by trauma and cytokines?
COX-1 is constitutive; COX-2 is induced by trauma, growth factors, and proinflammatory cytokines.
95
What clinical reason is given for COX-2 selective inhibitors being advantageous in dogs?
They are associated with a lower incidence of gastric ulceration compared to nonselective inhibition.
96
Which pathway primarily produces leukotrienes and which cell types are highlighted as major producers?
LOX pathway; leukocytes are primary producers, with contributions from platelets and endothelial cells.
97
What is the primary role of leukotrienes in inflammation as stated?
They are proinflammatory mediators that regulate leukocyte trafficking and blood flow.
98
What are pro-resolution eicosanoids and what key conceptual distinction from immunosuppression is emphasized?
Endogenously produced mediators (e.g., lipoxins; resolvins/protectins from omega-3 PUFAs) that promote return to homeostasis; they are not immunosuppressive.
99
What functional switch is described as initiating production of pro-resolution mediators within hours?
A PGE2 and PGD2-mediated switch that redirects mediator production toward resolution.
100
What is platelet activating factor (PAF) derived from and what is its relationship to the arachidonic acid pathway?
It is metabolized from membrane phospholipids via phospholipase A2 and stimulates AA release, increasing eicosanoid production.
101
List two leukocyte/platelet effects of PAF described in the notes.
It increases neutrophil integrin affinity to enhance adhesion/motility/degranulation and enhances platelet aggregation and degranulation.
102
Which two broad categories of effects of reactive oxygen species (ROS) are emphasized in the notes?
Beneficial effects in antimicrobial defense/debridement/signaling, and pathologic effects causing tissue damage.
103
Name two physiologic sources of ROS described in the notes.
Mitochondrial electron transport during ATP generation and phagocytic oxidative burst.
104
Name two clinical/surgical pathologies associated with excessive ROS listed in the notes.
Pancreatitis, adhesion formation, delayed wound healing, and excessive scarring (any two).
105
Which scenario is highlighted as producing large amounts of ROS via lipid peroxidation?
Prolonged ischemia followed by reperfusion and oxygen delivery, producing unrestricted ROS and peroxidation of membrane phospholipids.
106
Name three antioxidant defenses listed as balancing ROS in the notes.
Vitamins A, C, and E; and glutathione peroxidase (any three).
107
Nitric oxide (NO) is synthesized from which amino acid by what enzyme family?
From arginine by nitric oxide synthase (NOS), with constitutive and inducible forms.
108
What is the primary physiologic function of NO emphasized in the notes?
Regulation of vascular tone via smooth muscle relaxation (vasodilation).
109
List two homeostatic protective effects attributed to constitutive NO in the notes.
Maintenance of vascular tone; inhibition of platelet aggregation/leukocyte adhesion; protective anti-inflammatory effects in the GI tract (any two).
110
List two proinflammatory roles of inducible NO (iNOS) described in the notes.
Enhances macrophage killing; promotes proinflammatory cytokine production; contributes to ROS and perpetuates inflammation when excessive (any two).
111
What is the nuanced point about NO and wound healing/tissue strength described?
NO can help tensile strength and collagen content, but excessive NO can impair healing by sustaining inflammation and ROS.
112
Which drugs are noted to inhibit sustained NO release in chronic inflammation?
Cyclosporine and steroids.
113
Carbon monoxide (CO) is produced through what normal metabolic pathway, and what happens to this system during inflammation?
CO is generated during heme breakdown to bilirubin; inducible heme oxygenase is upregulated during inflammation, increasing CO.
114
List two anti-inflammatory effects of carbon monoxide described in the notes.
Upregulates IL-10, downregulates proinflammatory cytokines, and decreases adhesion molecule expression on endothelial cells and neutrophils (any two).
115
Hydrogen sulfide is produced during what metabolism and what is its key effect on smooth muscle?
Produced during cysteine metabolism and by intestinal bacterial flora; it relaxes smooth muscle via ATP-dependent K+ channels causing vasodilation and promotes resolution.
116
Which cytokines are listed as stimulating hepatocyte production of acute phase proteins?
IL-6 and IL-1, IFN-γ, and TNF-α.
117
What is the major negative acute phase protein listed in the notes?
Albumin.
118
What defines a 'positive acute phase protein' in the notes, and what is the typical time course of their rise?
They increase by ≥25% during inflammation; they peak at ~24–48 hours and remain elevated while inflammatory stimuli persist.
119
What are two listed functions of C-reactive protein (CRP) in the acute phase response?
Binds bacteria and necrotic/apoptotic cells; activates complement; promotes inflammatory cytokines and leukocyte chemotaxis (any two).
120
Which cells are listed as producers of serum amyloid A (SAA) and what is one function described?
Produced by macrophages, endothelial cells, and hepatocytes; aids cholesterol clearance from macrophages after phagocytosis and is chemoattractive for immune cells.
121
All complement activation pathways converge on cleavage of which component, producing what two key fragments?
Cleavage of C3 into C3b and C3a.
122
What are two broad outcomes of complement activation highlighted in the notes?
Facilitates inflammation and pathogen removal via opsonization/phagocytosis and membrane attack complex (MAC) formation.
123
What proinflammatory role of thrombin is highlighted in the notes?
Thrombin promotes synthesis of prostaglandins, nitric oxide, and PDGF, and stimulates proinflammatory cytokine release.
124
Why is inflammation described as pro-thrombotic in the notes?
It increases vWF and endothelial tissue factor expression and impairs fibrinolysis (reduced plasmin activation), while reducing anticoagulant pathways (e.g., ATIII, protein C).
125
The kallikrein–kinin system is activated simultaneously with coagulation through activation of which factor?
Factor XII.
126
What are the key vascular and sensory effects of bradykinin described in the notes?
It stimulates vasodilation via NO release, increases vascular permeability, and produces pain.
127
Which neuropeptide is identified as a major tachykinin and what two proinflammatory effects are listed?
Substance P; it promotes pain transmission and induces prostaglandin release and leukocyte chemotaxis.
128
What defines sepsis in the notes, relative to SIRS?
Sepsis is SIRS plus infection.
129
What physiologic parameters are listed as commonly aberrant during systemic inflammation (SIRS)?
Body temperature, heart rate, blood pressure, respiratory rate, and leukocyte counts.
130
How is multiple organ failure (MOF) defined in the notes?
Progressive dysfunction of two or more organ systems not involved in the initial insult, due to major self-destructive inflammation.
131
What pathophysiologic hypothesis is proposed in the notes for the origin of mediators driving MOF?
Reperfusion-mediated oxidative injury to the gut generates mediators that drive systemic inflammation and organ dysfunction.
132
Describe the 'two-hit' phenomenon as presented in the notes.
An initial event primes neutrophils/macrophages, leading to an exaggerated response to subsequent insults (e.g., infection, surgery, ventilation, treatment).
133
How do SIRS and the compensatory anti-inflammatory response relate temporally, and what adverse outcome can result?
They occur concurrently; an overwhelming anti-inflammatory response can cause immunosuppression and increased susceptibility to infection.
134
What is endotoxin tolerance (cross tolerance) in the context of chronic inflammation?
A phenomenon where prior endotoxin exposure reduces responsiveness to subsequent endotoxin or related stimuli, contributing to immune dysregulation.
135
Which histologic/biologic features characterize chronic inflammation in the notes?
Prolonged inflammation with monocytic infiltrates, angiogenesis, and progressive tissue fibrosis due to fibroblast–inflammatory cell crosstalk.
136
What is a common trigger for granulomatous inflammation mentioned in the notes that is highly relevant to surgery?
Foreign bodies such as suture material (also infectious agents/toxins).
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