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POS Flashcards > Red - Immune Cells > Flashcards

Red - Immune Cells Flashcards

1
Q

What is an endotoxin?

A
  • Cell wall component of gram-neg bacteria

- Potent mediator of septic shock

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2
Q

What region of endotoxins is most responsible for their toxicity?

A
  • Lipipolysaccharide consisting of:
    1) O-Antigen/Side Chain
    2) Core
    3) Lipid-A

*Lipid-A = region most responsible

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3
Q

What is the host response to endotoxins?

A
  • Activation of macrophages
  • Activation of complement cascade
  • Activation of coagulation cascade
  • Release of TNF-alpha, IL-1, IL-6, PAF, NO, various oxidants
  • Renal failure (nephrotoxin)
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4
Q

What activates the complement cascade?

A
  1. Classical pathway: Fe regions IgG/IgM
  2. Alternative pathway: directly by sp. pathogens
  • Infection
  • Shock
  • Tissue Injury
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5
Q

What are the most potent components of the complement cascade?

A
  • C3a

- C5a

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6
Q

What are the effects of C3a and C5a?

A
  • C3a, C4a, C5a = anaphylatoxins, proteins bind surface mast cells/basophils–>cell degranulation
  • release of histamine from basophils and mast cells: vasodilation, increased permeability (allows IgG/complement to leave blood–>tissues), bronchoconstriction
  • C5a = chemoattractant for neutrophils and mononuclear phagocytes
  • Stimulate IL-1 release
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7
Q

What are eicosanoids?

A

Inflammatory mediators primarily generated by hydrolysis of membrane phospholipids by phospholipase A2 + converted to: leukotrienes, PG, prostacyclin, thromboxane families
- Not stored in cells. Generated rapidly.

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8
Q

How are eicosanoids derived?

A
  • Phospholipid–>ArAc (via phospholipase)
  • ArAc–>LT (via lipoxygenase) = LT inhibs, glucocorticoids
  • ArAc–>PG/TX/PC (via COX)

PH Inihib = glucocorticoids, NSAIDS
TX inhibit = NSAIDS
PC Inhibit = NSAIDS

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9
Q

What are leukotrienes produced by?

A

Mast cells
Macrophages
Neutrophils
Vascular smooth muscle cells

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10
Q

What are the effects of LT B4?

A
  • Chemoattractant for neutrophils
  • Promotes neutrophil adhesion

Hemorrhagic shock: Acute lung injury, AKI

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11
Q

What are the effects of LT C4, LT D4, and LT E4?

A
  • Bronchoconstriction
  • Vasoconstriction
  • Increased vascular permeability
  • Neutrophil chemoattractant
  • Leukocyte adherence
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12
Q

What are the effects of PG E2?

A
  • Vasodilation
  • Bronchodilation
  • Pyrexia
  • Immunodepression by inhibiting TNF-alpha and IL-1 synthesis
  • Suppresses effector function of macrophages
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13
Q

What are the effects of prostacyclins (PG12)?

A
  • Produced largely by vascular endothelium
  • Vasodilation
  • Bronchodilation
  • Inhibition of platelet aggregation

*Inhibited by glucocorticoids

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14
Q

What are the effects of thromboxane A2?

A
  • Produced mainly by platelets
  • Vasoconstriction
  • Bronchoconstriction
  • Platelet aggregation
  • Potent constrictor of smooth muscle
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15
Q

What are kinins implicated in?

A
  • Inflammation
  • Anaphylaxis
  • Septic shock
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16
Q

What are the principal effects of kinins?

A
  • Vasodilation
  • Increased capillary permeability
  • Pain
  • Tissue edema
  • Stimulate production of NO: vasodilation and decreased platelet aggregation
  • Activation of phospholipase and thus amplification of inflammatory response (ArAc)
  • Potent bronchoconstriction
  • Increase renal vasodilation: decrease renal perfusion pressurere–> decrease BP
17
Q

What are the effects of histamine?

A
  • Vasodilation
  • Increased permeability
  • Bronchoconstriction
18
Q

What are the cytokines?

A

Protein messenger molecules made by immune cells to facilitate communication and orchestrate an attack

  • interleukins
  • IFNs
  • TNFs
  • CSFs
  • TGFs
19
Q

How do cytokines function?

A

Act directly on target cells and potentiate each other to amplify host response

Paracrine
Autocrine
Synergy
Pleotrophy

20
Q

What are the effects of NO?

A
  • Vasodilation
  • Inhibition of platelet aggregation
  • Also seem to be involved in pathophysiologic decrease in BP and SVR seen in sepsis
21
Q

What is IL-1 produced by?

A
  • Primarily monocytes and tissue macrophages (important stimulus = microbial products)
  • Neutrophils
  • Lymphocytes
  • Endothelial cells
  • Keratinocytes
22
Q

What stimulates the release of IL-1?

A
  • Microbe particles
  • Ag-Ab complexes
  • Ig
  • C5a (opsonization)
  • Other cytokines
  • TGF- beta
23
Q

What are the effects of IL-1?

A
  • Fever (via effect on hypothalamus)
  • Stimulation of T and B lymphocytes (promote maturation and clonal proliferation)
  • Acute phase protein production and release
  • Stimulates pit stress hormone release
  • Myocardial depression
  • Regulates skeletal muscle proteolysis in sepsis
  • Potentiation of other inflammatory mediator release
  • Chemoattraction of leukocytes
  • Promotion of endothelial cell procoagulant effects
  • Helps activate Th cells by acting as a costimulator and antigen presenting cell receptors
24
Q

What is IL-6 produced by?

A
  • Monocytes and macrophages
  • Neutrophils
  • Fibroblasts

Bone marrow cells

25
Q

What are the effects of IL-6?

A
  • Induces fever
  • Promotes T and B cell activates: acts on proliferating B cells to promote differentiation–>plasma cells
  • Stimulates acute phase protein synthesis by liver
  • Stimulate antibody secretion
  • Regulates hepatic response to inflammation–>CRP!!
26
Q

What is TNF-alpha secreted by?

A
  • monocytes and macrophages primarily
  • lymphocytes
  • mast cells
  • kupffer cells
  • glial cells
27
Q

What stimulates TNF-alpha production?

A
  • Endogenous and exogenous factors from microbes
  • Endogenous and exogenous factors from tumors
  • The most important mediator of septic shock and MODS (multiple organ dysfunction syndrome)
28
Q

What are the local effects of TNF-alpha?

A

Leukocytes chemoattraction

  • Binds to TNF receptor on cells–>activates cascade pathway–>apoptosis
  • Inflam–>recruits neutrophils, monocytes, T cells, NK cells by inducing changing in vascular endothelial cell adhesion
  • IFN-y potentiates TNF-alpha effects
  • Overproduction–>excessive tissue destructive inflammation (ie arthritis and septic shock)
29
Q

What are the effects of TNF-alpha of exaggerated systemic levels?

A

Acts on hypothalamus

  • Fever
  • Release of stress hormone (catecholamines, glucagons, cortisol)
  • Myocardial depression
  • Increased systemic and pulmonary vascular permeability
  • Hypotension
  • Lactic acidosis
  • DIC
30
Q

What are the effects of platelet activating factor?

A

Similar to histamine but longer acting

  • Amplifies action of TBF-alpha and IL-1 (from platelet activation)
  • Leukocyte activation, adherence, motility, chemotaxis, invasion
  • Stimulates synthesis of leukotrienes
  • Platelet aggregation
  • Bronchoconstriction
  • Increased vascular permeability
  • Cardiodepression
  • Hypotension
31
Q

What are oxidants produced by?

A

Activated neutrophils among other cells

32
Q

What are the effects of oxidants?

A
  • Lipid per oxidation and membrane disruption causing cell death
  • oxidative damage to DNA
  • oxidative damage to amino acids and proteins
  • Inhibition of ATP synthesis in both glycolytic and mitochondrial pathway
  • Reduction in cellular levels of NADH
  • Interference of intracellular calcium regulation
33
Q

What are the effects of EPI and NE?

A
  • Tachycardia
  • Increased inotropy
  • Peripheral vasoconstriction
  • Increased metabolic rate
  • Increased glycogenolysis and increased gluconeogenesis: hyperglycaemia
  • Inhibition of insulin secretion
34
Q

What are the effects of cortisol?

A

Glucocorticoid

  • Lipolysis
  • Proteolysis
  • Gluconeogenesis

Primarily a catabolic steroid: inhibits lipoxygenase and COX (eicosanoid pathway)

35
Q

What are the effects of glucagon?

A
  • PEptide hormon
  • Produced by pancreatic alpha cells
  • Gluconeogenesis: increased glucose

POS Flashcards (7 decks)

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