Ch. 2: Systemic inflammatory response Flashcards
Define SIRS
Systemic inflammatory response syndrome is the body ́s response to infection and injury resulting in an incongruous and exaggerated systemic inflammatory reaction. SIRS can be triggered by infection, endotoxemia, or noninfectious insults, such as severe trauma, ischemia, immune-mediated disease, surgery, hypothermia, hyperthermia, or intense hypoxemia.
Define CARS
Compensatory anti-inflammatory response syndrome is the over-recruitment of anti-inflammatory processes such as cytokines, soluble cytokine receptors, receptor antagonists, prostaglandin E2, and corticosteroids. It is a state of anergy, increased susceptibility to infection, and inability to repair damaged tissues ensues.
Define MARS
Mixed anti-inflammatory response syndrome is the surges of both SIRS and CARS coexist. In the equilibrium, if SIRS and CARS are ultimately appropriately balanced, then homeostasis resumes.
Match the cytokines to the right cells:
a. TNF
b. IL-1
c. IL-6
d. IL-6
e. INF-y
- Endothelial cells
- Monocytes
- Keratinocytes
- Fibroblast
- Macrophages
- Neutrophils
- Lymphocytes
- Natural killer cells
Endothelial cells (IL-1, IL-8)
Monocytes (TNF, IL-1, -6, -8, INT-y)
Keratinocytes (IL-1, IL-6)
Fibroblasts (IL-1, IL-6)
Macrophages (TNF, IL-1, -6, -8, INT-y)
Neutrophils (TNF)
Lymphocytes (IL-1, IL6)
Natural killer cells (TNF, INF-y)
What is not a function of TNF, IL-1 and IL-6?
a.Initiate coagulation
b.Fibrinolysis
c.Promote platelet aggregation d.Complement activation
e.Neutrophil chemotaxis
c. Promote platelet aggregation
Anti-inflammatory cytokines are released from?
a.Monocytes, endothelial cells, lymphocytes
b.Monocytes, macrophages, natural killer cells
c.Monocytes, natural killer cells, fibroblasts
d.Monocytes, macrophages, t-helper cells
d.Monocytes, macrophages, t-helper cells
What are the action of anti-inflammatory cytokines?
a. Inhibiting macrophage activation, proinflammatory cytokine release, antigen-presenting cells, and increase chemotaxis.
b. Increase macrophage activation, proinflammatory cytokine release, and inhibiting antigen-presenting cells, and chemotaxis
c. Inhibition of macrophage activation, proinflammatory cytokine release, antigen-presenting cells, and chemotaxis.
d. Increase macrophage activation, inhibit proinflammatory cytokine release, promote antigen-presenting cells, and inhibition of chemotaxis.
c. Inhibition of macrophage activation, proinflammatory cytokine release, antigen-presenting cells, and chemotaxis.
Define PAMPs and DAMPS
PAMPs: pathogen-associated molecular pattern, activates innate immune system
DAMPs: damage-associated molecular pattern, activates innate immune system
Prostanoids are released when arachidonic acid is metabolized by cyclooxygenase, match the right prostanoid to its function:
a.Tromboxane A2 (TxA2)
b. PGI2
c. PGE2
- Vasodilator and a pyrogen
- Vasoconstriction and platelet aggregation
- Vasodilation and inhibits platelet aggregation
a.Tromboxane A2 (TxA2) Vasoconstriction and platelet aggregationb.PGI2 Vasodilation and inhibits platelet aggregationc.PGE2Vasodilator and a pyrogen
Choose the false statement for serum amyloid A (SAA)
a. Involved in cholesterol regulation, chemotaxis, and mediation of anti-inflammatory events
b. Increase vascular permeability, platelet aggregation and activation of phagocytes.
c. May increase 100-fold during the acute phase response
d. Main site of synthesis is the liver.
b. Increase vascular permeability, platelet aggregation and activation of phagocytes.
What are Reactive Oxygen Species?
All oxygen-derived toxic mediators that most commonly originate form mononuclear phagocytes or neutrophils. Oxygen free radicals are oxygen-containing molecules that contain an unpaired electron. They can react with essentially any molecular component in their quest to “re-pair” the unpaired electron.
Match vasoactive mediators to effects
a.Complement components
b.PGs
c.TxA2
d.PAF
e.Angiotensin
f.Bradykinin
g.Leukotrienes
a.Complement components: Vasodilation (PGs, Histamine, NO)
b.PGs: Vasoconstriction (Angiotensin, Endothelin, TxA2, leukotrienes)
c.TxA2: Increase vascular permeability (Complement components, NO, Bradykinin, PAF, leukotrienes)
d. PAF: Decrease vascular permeability
e. Angiotensin
f. Bradykinin
g. Leukotrienes
What are the diagnostic criteria for SIRS in adult horses?
a. Rectal temperature: >38.5 or <37.0
b. Heart Rate: >52bpm
c. Respiratory rate: >20breaths/min or PaCO2 <32mmHg
d. White blood cell count: >12,500/uL or <5000/uL or 10% bands
e. Mucous membrane color
f. Blood Lactate values: >2.06mmol/L
Define MODS
Multiple organ dysfunction syndrome refers to the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.
What is the difference between primary and secondary MODS
a. Primary MODS are any disease process including a well-defined injury that affects the function of organs at the initial site of insult
b. Secondary MODS is when organs remotely positioned form the primary injury, not as a direct response to the insult, but as a consequence of the host ́s response to the injury.
What is the pathophysiological reason for DIC?
Disseminated intravascular coagulopathy occurs due to prolonged or excessive thrombi formation. Leading to the consumption of platelets, coagulation, anticoagulation, and fibrinolytic factors. Thus balance is lost, and hemorrhage ensue.
Antithrombin (AT) and protein C anti-inflammatory effects, choose the false statement:
a. Induction of prostacyclin synthesis
b. Reduction of chemotaxis and neutrophil adhesion
c. Diminution of endotoxin-induced cytokines
d. Enhances opsonization of both microbes and damaged host cells.
d. Enhances opsonization of both microbes and damaged host cells.
What are the triggers for ALI and ARDS?
a. Sepsis, aspiration of gastric content, smoke inhalation, severe trauma, and transfusion reaction
b. Sepsis, aspiration of gastric content, burns, and transfusion reaction
c. Sepsis, severe trauma, exhaustion, and long travels, air embolism.
d. Sepsis, aspiration of gastric content, abdominal distension, left sided hear failure.
a. Sepsis, aspiration of gastric content, smoke inhalation, severe trauma, and transfusion reaction
What happens during acute lung injury and acute respiratory distress syndrome?
Injury to the alveoli and pulmonary endothelium causes thromboembolism and protein-rich pulmonary edema. Subsequently, type II pneumocytes and fibroblasts are recruited to replace damaged areas in the alveoli. Collectively, these injuries severely impairs gas exchange.
What is the mechanisms of Critical illness related corticosteroid insufficiency (CIRCI)?
Cytokine induced inhibition of any component of the hypothalamic-pituitary-adrenal axis, downregulation and sensitivity of tissue cortisol receptors, and direct inflammatory, hemorrhagic, or hypoxic damage to the adrenal gland (Waterhouse-Friderichsen syndrome).
What is the correct respiratory criteria for MODS?
a. Acute onset (<72 hours) of respiratory distress, no known risk factors for ALI or ARDS, pulmonary capillary leakage with decreased pulmonary capillary pressure, and inefficient gasexchange
b. Acute onset (<48 hours) of respiratory distress, a known risk factor for ALI or ARDS, pulmonary capillary leakage with increased pulmonary capillary pressure, and inefficient gas exchange
c. Acute onset (<72 hours) of respiratory distress, a known risk factor for ALI or ARDS, pulmonary capillary leakage without increased pulmonary capillary pressure, and inefficient gas exchange
d. Acute onset (<24 hours) of respiratory distress, no known risk factors for ALI or ARDS, pulmonary capillary leakage without increased pulmonary capillary pressure, and inefficient gas exchange
c. Acute onset (<72 hours) of respiratory distress, a known risk factor for ALI or ARDS, pulmonary capillary leakage without increased pulmonary capillary pressure, and inefficient gas exchange
What are the cardiovascular criteria for MODS?
Lactatemia, hypotension, pathological (ventricular) arrhythmias, myocardial ischemia (increased troponin), loss of heart rate variability, decreased cardiac output and contractility.
What are PAMPs and what are the common types?
PAMPs are pathogen-associated molecular patters, which are expressed by pathogens and can be bound to pattern-recognition receptors. Common PAMPs include bacterial cell wall extracts such as endotoxin, peptidoglycan and lipoteichoic acid, and prokaryotic DNA.
Pattern-recognition receptors are divided into groups, what are they?
Secreted PRR, cell membrane PRRs involved in phagocytosis, and cell membrane PRRs involved in signal transduction.
