Inflammation and Hemostasis (Lecture 31)
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1
What is the main focus of Lecture 31?
The relationship between inflammation and hemostasis, including how immune responses promote coagulation.
2
What clinical abnormalities did Quinter, the 7.5-year-old dog, present with?
Fever, thrombocytopenia, right pelvic limb lameness, lethargy, decreased appetite, and increased respiratory rate.
3
What were the major CBC abnormalities in Quinter?
Mild normocytic normochromic anemia, marked neutrophilia with a toxic left shift, and severe thrombocytopenia.
4
What is the relationship between inflammation and hemostasis?
They are tightly interconnected and can activate and amplify each other.
5
What is immunothrombosis?
An innate immune mechanism that uses localized coagulation to help defend against pathogens.
6
What are the protective functions of immunothrombosis?
Trap pathogens, prevent their spread, promote localized killing, and minimize host damage.
7
Which receptors recognize PAMPs and DAMPs to initiate inflammatory signaling?
Toll-like receptors (TLRs) and other pattern recognition receptors.
8
What examples of PAMPs and DAMPs are given in the lecture?
PAMPs include LPS, flagellin, and LTA; DAMPs include heat shock proteins.
9
What happens after TLRs recognize PAMPs or DAMPs?
Proinflammatory signaling pathways activate, causing inflammatory cytokine secretion.
10
Which complement fragments connect inflammation to hemostasis?
C3a and C5a, which are proinflammatory mediators.
11
How do C3a and C5a promote coagulation?
C3a activates platelets; C5a increases tissue factor expression by monocytes.
12
How do negatively charged molecules such as DNA and RNA promote coagulation?
They can activate factor 12 through contact activation.
13
Where is tissue factor (TF) normally expressed?
On subendothelial cells beneath the vascular endothelium.
14
What inflammatory signals increase monocyte tissue factor expression?
PAMP/DAMP recognition, complement components, inflammatory cytokines, and reactive oxygen species.
15
What is the role of tissue factor pathway inhibitor (TFPI) during inflammation?
It inhibits tissue factor-mediated coagulation
16
What are neutrophil extracellular traps (NETs)?
Extracellular networks of DNA and histones released by activated neutrophils.
17
How do NETs contribute to innate immunity?
They physically trap microbes and contain antimicrobial peptides.
18
How do NETs provide a scaffold for thrombosis?
Their extracellular DNA and histone networks provide a structure for thrombus assembly.
19
How do histones released during NETosis promote coagulation?
They activate platelets.
20
Which coagulation factor is activated by NETs?
Factor 12.
21
How do NETs interfere with natural anticoagulant mechanisms?
They inhibit TFPI and block the thrombomodulin–activated protein C pathway.
22
What are microparticles (MPs)?
Small membrane-bound vesicles released from cells.
23
Which cells produce most circulating microparticles?
Platelets and megakaryocytes.
24
Which cell-derived microparticles may be especially rich in tissue factor?
Leukocyte-derived and endothelial cell-derived microparticles.
25
What conditions stimulate microparticle release?
Stress, hypoxia, reactive oxygen species, ischemia, and inflammation.
26
How do microparticles contribute to inflammation?
They promote complement activation, leukocyte adhesion, cytokine release, and changes in endothelial function.
27
Why does congenital factor 12 deficiency in cats not typically cause severe bleeding?
Factor 12 is not essential for normal in vivo hemostasis but contributes to contact activation and immunothrombosis.
28
Which animal groups naturally lack factor 12?
Birds, reptiles, and marine mammals.
29
What are the three major components of the contact activation pathway?
Factor 12, plasma prekallikrein (PPK), and high-molecular-weight kininogen (HK).
30
How is factor 12 initially activated during contact activation?
It undergoes inefficient autoactivation after contacting negatively charged surfaces.
31
How does kallikrein connect contact activation to innate immunity?
It can activate the complement system.
32
How does thrombin connect coagulation to inflammation?
It activates protease-activated receptors (PARs) on platelets, endothelial cells, and other cells.
33
What effects does thrombin have on platelets through PAR activation?
Platelet shape change, activation, and degranulation.
34
Why can severe inflammation lead to pathological thrombosis?
Inflammation activates platelets, tissue factor, NETs, microparticles, and contact activation while suppressing anticoagulant mechanisms.
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