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Systemic Inflammatory Response Flashcards

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1
Q

T/F: Phagocytic activation of neutrophils is directly responsible for the development of clinical signs and symptoms of SIRS.

A

False; Phagocytic activation of the monocyte/ macrophage cell lineage is directly responsible for the development of clinical signs and symptoms

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2
Q

T/F: It is generally accepted that bacteria or their endotoxins, or both, induce and sustain a marked inflammatory response by the host, which eventually overwhelms sensitive organs and often results in a fatal outcome.

A

True

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3
Q

Which of the following is Not one of the immune system goals in response to microbial invasion?

  1. deprive invading organisms of nutrition
  2. contain infection
  3. alarm the host to defend against infection
  4. promote tissue repair
A
  1. it does not deprive nutrition
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4
Q

Which inflammatory cytokines promote pyrogenic activity?

A

TNF and interleukin 1

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5
Q

What are some of the main functions of TNF, Il-1, and Il-6?

A

Pro-inflammatory cytokines: they initiate coagulation, fibrinolysis, complement activation, the acute phase response, and neutrophil chemotaxis. TNF and Il-1 also induce pyrogenic activities and augment further cytokine production.

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6
Q

______________ and ______________ are universal sources for the pro-inflammatory cytokines

A

monocytes and macrophages

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7
Q

Monocytes and macrophages are universal sources for the pro-inflammatory cytokines, though other cell types contribute as well. What are the other cells types and which cytokines do they contribute?

A

Neutrophils (TNF);
endothelial cells (Il-1, Il-8); fibroblasts, keratinocytes, and lymphocytes (Il-1, Il-6);
natural killer cells (TNF, INF-γ).

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8
Q

What are the main sources for anti-inflammatory cytokines?

A

monocytes, macrophages, and T-helper cells

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9
Q

In what ways do anti-inflammatory cytokines serve to restrain inflammation?

A

inhibiting macrophage activation, proinflammatory cytokine release, antigen-presenting cells, and chemotaxis.

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10
Q

T/F: platelet-activating factor (PAF) is released from cell membrane (mononuclear phagocytes, endothelial cells, and platelets) phospholipids by phospholipase A2.

A

True; The released alkyl-lyso-glycerophosphocholine is then acetylated to form PAF.

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11
Q

T/F: The biologic effects of PAF include vasoconstriction, reduced vascular permeability, platelet aggregation, and recruitment and activation of phagocytes. It also is a positive inotrope.

A

False; The biologic effects of PAF include Vasodilation, Increased vascular permeability, platelet aggregation, and recruitment and activation of phagocytes. It also is a Negative inotrope.

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12
Q

The expected serum amyloid A concentration in healthy neonatal foals and adult horses is less than _____.

A

27 mg/L

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13
Q

What are the cells of origin for TNF?

A

monocytes/macrophages, neutrophils, and natural killer cells

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14
Q

What are the cells of origin for Interleukin-1?

A

monocytes/macrophages, endothelial cells, lymphocytes, fibroblasts, keratinocytes

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15
Q

What are the cells of origin for Interleukin-6?

A

monocytes/macrophages, lymphocytes, fibroblasts, keratinocytes

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16
Q

What are the cells of origin for Interleukin-8?

A

monocytes/macrophages, endothelial cells,

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17
Q

What are the cells of origin for Interferon-γ (inf-γ)?

A

monocytes/macrophages, natural killer cells

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18
Q

Where is arachidonic acid released from?

A

arachidonic acid is a 20-carbon fatty acid that is a major constituent of the phospholipids of all cell membranes. Phospholipase A2 is the enzyme responsible for cleavage of arachidonic acid.

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19
Q

What is the role of arachidonic acid?

A

it serves as the parent molecule for eicosanoid synthesis.

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20
Q

Once released, arachidonic acid is further metabolized by either ____________, to form the family of leukotrienes, or ________________, to form the prostanoids: _______________ and the __________________.

A

lipoxygenase; cyclooxygenase; thromboxane A2 (TxA2); prostaglandins (PGs)

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21
Q

What are the biologic effects of platelet-activating factor (PAF)?

A

vasodilation, increased vascular permeability, platelet aggregation, recruitment and activation of phagocytes; negative inotrope

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22
Q

Where is the key site for acute phase protein production?

A

liver

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23
Q

T/F: The serum concentrations of the major acute phase proteins, serum amyloid A (SAA) and C-reactive protein (CRP) can each increase as much as 100 fold during the acute phase response.

A

True

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24
Q

The ____________ _________ is represented by the acute phase synthesis of C3a, C4a, C5a, C4b, C3b, C5b-C9, factor B, and C1 inhibitor. Collectively, these compounds induce ____________, increase vascular permeability, are chemotactic for neutrophils, and enhance opsonization of both microbes and damaged host cells.

A

complement system; bacteriolysis;

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25
Q

Balanced activation of the __________ and __________ systems by the acute phase response of factor VIII, fibrinogen, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor, fibronectin, von Willebrand factor, and tissue factor leads to formation of intravascular and extravascular __________ that capture and contain infectious organisms and inflammatory debris and provide a scaffold for ________ ___________.

A

coagulation; fibrinolytic; “clots”; tissue repair

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26
Q

T/F: The release of the acute phase transport and scavenger proteins, such as ceruloplasmin, haptoglobin, lipopolyscharride-binding protein, soluble cluster of differentiation antigen 14 (CD14), and lactoferrin, bind bacterial nutrient components, such as copper and iron, and neutralize or transport toxic bacterial components.

A

True

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27
Q

Free radicals can react with essentially any molecular component in their quest to “repair” the unpaired electron. In doing so, more radicals are generated and molecular damage ensues with loss of _______ function, cross-linking of DNA, lipid__________, vaso-_________, and pain. Oxygen free radicals also induce _________ production and endothelial adhesion molecules.

A

protein; peroxidation; vasoconstriction; cytokine

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28
Q

T/F: The reactive oxygen species encompass all oxygen-derived toxic mediators that most commonly originate from lysis of bacterial cell walls.

A

False; The reactive oxygen species encompass all oxygen-derived toxic mediators that most commonly originate from mononuclear phagocytes or neutrophils.

29
Q

T/F: Other reactive oxygen species that do not contain unpaired electrons include hydrogen peroxide (H2O2) and nitric oxide (NO). NO is generated enzymatically in phagocytes by inducible no synthetase, which is activated by endotoxin and cytokines.

A

True

30
Q

Angiotensin, endothelin, TxA2, and leukotrienes (LTC4, D4, and E4) have vaso-________ activities.

A

vasoconstrictive

31
Q

In addition to the prostaglandins and NO, bradykinin, a by-product of activation of the contact coagulation system, and histamine are vaso-_______.

A

vasodilators

32
Q

PAF, leukotrienes, complement components (C3a, C5a), NO, and bradykinin have what effect on vascular permeability?

A

they promote vascular leakage

33
Q

What are the 4 clinical manifestations of SIRS (adjusted to horses)? how many need to be present to diagnose SIRS?

A
  1. body temp > 38.6° C (101.5° F) or < 36.6° C (98° F);
  2. heart rate > 60 bpm (25% increase over the high end of the normal avg HR);
  3. tachypnea (RR > 20 bpm), or hyperventilation (PaCO2 < 32 mmHg;
  4. white blood cell count, > 14,000/ ml, < 4000/ml, or more than 10% immature neutrophils (“bands”).

Need at least two of these criteria to diagnose SIRS.

34
Q

T/F: The treatment of SIRS is largely directed at controlling the primary disease process that triggered the response.

A

True

35
Q

___________ _________ ________ _________ refers to the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.

A

multiple organ dysfunction syndrome (MODS)

36
Q

When the response to infection and injury results in an incongruous and exaggerated systemic inflammatory reaction, the clinical state is referred to as the __________ ___________ _______ _________ which can be initiated by infection, endotoxemia, or noninfectious insults, such as severe trauma, ischemia, immune-mediated disease, surgery, hypothermia, hyperthermia, or intense hypoxemia (i.e., hemorrhagic shock).

A

systemic inflammatory response syndrome, or SIRS

37
Q

What organ system is most often the cause of SIRS and MODS?

A

Gastrointestinal

38
Q

What are the three major elements that define dysfunction of the coagulation system associated with the development of MODS?

A

(1) excessive procoagulation, (2) loss of controlled fibrinolysis, and (3) loss of natural anticoagulant activities.

These events promote clot formation, especially in the microvascular space, which contributes to reduction of blood flow to vital tissues. With prolonged or excessive thrombi formation, platelets, coagulation, anticoagulation, and fibrinolytic factors are consumed, balance is lost, and hemorrhage may ensue. This state of clinical coagulopathy is referred to as DIC.

39
Q

Explain how MODS can lead to DIC.

A

MODS initially promotes clot formation, especially in the microvascular space, which contributes to reduction of blood flow to vital tissues. With prolonged or excessive thrombi formation, platelets, coagulation, anticoagulation, and fibrinolytic factors are consumed, balance is lost, and hemorrhage may ensue. This state of clinical coagulopathy is referred to as DIC.

40
Q

What are the percentages of clinical occurrence of DIC on admission for the following:
Colitis
Colonic torsion
Septic foals

A

Colitis –> 30%
Colon torsion –> 70%
Septic foals –> 25%

41
Q

T/F: The primary mechanism responsible for the initial hypercoagulative state of DIC is activation of the extrinsic coagulation cascade via enhanced expression of membrane tissue factors (i.e., thromboplastin).

A

True

42
Q

T/F: In horses, endotoxin appears to favor activation of plasminogen activator inhibitor (PAI) over tissue plasminogen activator (tPA).

A

True; These types of responses would be expected to enhance clot formation and be negatively correlated with prognosis for survival in equine colic patients.

43
Q

T/F: The natural anticoagulants antithrombin (AT) and protein C are rapidly consumed in sepsis or inactivated by neutrophil enzymes released during the inflammatory response.

A

True; AT and protein C also have several antiinflammatory effects, including induction of prostacyclin synthesis, diminution of endotoxin-induced cytokine and tissue factor synthesis, and reduction of chemotaxis and neutrophil adhesion.

44
Q

What are the ultimate consequences of insufficient AT and protein C activity?

A

increased clot formation and heightened inflammatory response

45
Q

T/F: Acute renal failure is defined as the presence of azotemia or oliguria, or both, in a normovolemic patient that does not have signs of postrenal obstruction.

A

True

46
Q

T/F: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) have been defined as the clinical conditions of acute onset of respiratory failure characterized by hypoxemia and diffuse bilateral pulmonary infiltrates on thoracic radiographs, with left atrial hypertension.

A

False: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) have been defined as the clinical conditions of acute onset of respiratory failure characterized by hypoxemia and diffuse bilateral pulmonary infiltrates on thoracic radiographs, in the absence of left atrial hypertension.

47
Q

What term is used to describe the clinical scenario in which the cortisol response is insufficient for the degree of stress induced by illness?

A

critical illness–related corticosteroid insufficiency (CIRCI)

48
Q

What condition should be suspected if three of the following conditions are seen: thrombocytopenia; prolonged prothrombin; activated partial thromboplastin time; decreased fibrinogen concentration or prolonged thrombin time; increased fibrin degradation products or D-dimer concentrations; or decreased antithrombin activity.

A

Disseminated intravascular coagulopathy (DIC)

49
Q

What is normal urine output in foals/neonates?

A

6 ml/kg/hr

50
Q

T/F: A main feature of the innate immune system that enables immediate discrimination is pattern-recognition receptors (PRRs) that are capable of detecting a variety of microbial ligands, referred to as pathogen-associated molecular patterns or PAMPs. Ultimately, the interaction of a PRR with its PAMP can directly neutralize the PAMP or microbe, or it may activate other components of the host immune system to deploy further defense mechanisms, initiate an inflammatory response, or commence tissue repair.

A

True

51
Q

T/F: A well-characterized cell signaling PRR-ligand relationship is CD14–Toll-like receptor (TLR) and its well-characterized PAMP, endotoxin.

A

True

52
Q

T/F: Endotoxin is a heat-labile toxin consisting of lipopolysaccharide comprising approximately 75% of the outer cell wall of gram-positive bacteria.

A

False; Exotoxin is heat-labile and actively secreted from gram positive bacteria. Endotoxin is a heat-stable toxin consisting of lipopolysaccharide comprising approximately 75% of the outer cell membrane of gram-negative bacteria.

53
Q

T/F: Bacteria do not actively secrete endotoxin. Rather, when gram-negative bacteria multiply or lyse upon bacterial cell death, endotoxin is released from the outer cell membrane.

A

True

54
Q

Endotoxin consists of three structural domains, what are they?

A

A highly variable outer polysaccharide “O-antigenic” region, a core region consisting mostly of monosaccharides, and the highly conserved toxic moiety, lipid A.

55
Q

T/F: Once in the blood, endotoxin’s amphipathic properties cause it to form aggregates resembling micelles that otherwise spontaneously disperse into monomers at a very slow rate.

A

True

56
Q

What is LBP and what is its function during endotoxemia?

A

Lipopolysaccharide binding protein (LBP) is a lipid transfer protein synthesized by the liver. It extracts molecules of endotoxin from aggregated micelles in the blood and transports them to various locations. Through its interaction with lipid A, LBP effectively imprisons endotoxin, with its potential for toxicity determined by the complex’s final destination. LBP can rapidly deliver monomers of endotoxin to the cell surface of host inflammatory cells to evoke an inflammatory response or it can be transferred to other neutralizing lipoproteins, such as high-density lipoprotein, for eventual removal from the blood.

57
Q

T/F: Once at the cell surface (primarily mononuclear phagocytes), endotoxin is transferred to CD14,
a well-conserved receptor attached by a glycosylphosphatidylinositol anchor.

A

True

58
Q

T/F: Mononuclear phagocytes (monocytes and macrophages) express abundant CD14, though other inflammatory cells also express minute amounts.

A

True

59
Q

T/F: cD14 is a 53-kDa glycoprotein that exists as both a cell membrane receptor (mCD14) and a soluble form (sCD14) in the circulation.

A

True; sCD14 is normally present in the circulation and has dual functions. It may bind and neutralize circulating endotoxin, thereby competing with membrane CD14. however, it may also enhance endotoxin’s toxic effects by transferring it to membrane CD14 or to cells that do not express it.

60
Q

What types of pathogens does CD14 bind to?

A

CD14 binds to isolated monomers of endotoxin, intact bacteria, and several components of gram-positive bacteria, including peptidoglycan and lipoteichoic acid.

61
Q

Which Toll-like receptor (TLR) is the most important isotype in the recognition of endotoxin? which primarily confers recognition of gram positive bacteria?

A

TLR type 4 (TLR4) appears to be the most important isotype in the recognition of endotoxin, whereas TLR type 2 primarily confers recognition of gram-positive bacteria.

62
Q

T/F: Most of the deleterious effects of endotoxin are the result of overzealous endogenous synthesis of proinflammatory mediators and initiation of SIRS.

A

True; The development of tolerance, or the tachyphylactic response to prolonged endotoxin exposure, has been linked to downregulation of TLR4 and CD14 mRNA.

63
Q

The ______ ________ phase of endotoxemia that is characterized by pulmonary hypertension (increased pulmonary arterial and wedge pressures and increased pulmonary vascular resistance) and ileus associated with increased levels of ____________, though other vasoconstrictors likely contribute.

A

early hyperdynamic phase; thromboxane A2

64
Q

The ____________ phase of endotoxemia is caused by decreased systemic vascular resistance from the release of prostaglandins and is affiliated with the onset of fever and hypotension.

A

hypodynamic phase
Mucous membranes are often hyperemic, and capillary refill time is prolonged. With reduced tissue perfusion, the classic “toxic line” develops. if hypotension advances, mucous membranes become diffusely congested, progressing to cyanosis and then a grayish-purple pallor.

65
Q

What is the gold standard for measurement of endotoxin?

A

Limulus amebocyte lysate (LAL) assay, has been used to detect endotoxin in the plasma, portal circulation, or peritoneal fluid of horses and foals with naturally occurring endotoxemia.

66
Q

T/F: One cardinal diagnostic marker of endotoxemia and acute overwhelming bacterial infection is profound neutropenia with toxic neutrophil morphology (basophilic cytoplasm, vacuolization, Döhle bodies) with a left shift.

A

True

67
Q

T/F: The bactericidal actions of certain drug classes, particularly the β-lactam family, may increase the release of endotoxin.

A

True, A&S pg 22

68
Q

What is the mechanism of action of polymyxin B?

A

Polymyxin B is a cationic antibiotic that, in addition to its bactericidal properties, also binds to and neutralizes endotoxin through direct molecular interactions with the lipid A region.

69
Q

What is the mechanism of action of flunixin meglumine in cases of endotoxemia?

A

Flunixin meglumine, a nonspecific cyclooxygenase inhibitor, is highly effective in preventing endotoxin-induced prostanoid synthesis and associated clinical signs of endotoxemia.

Surgical Biology (8 decks)

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