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advance pathophys > chapter 6 innate immunity > Flashcards

chapter 6 innate immunity Flashcards

1
Q

physical barriers–epithelial cells

A 
skin sloughs off microorganisms.  
	Upper resp tract traps them by producing mucous , cough, sneeze.
	 GI—vomiting/defacation.  
	Urinary tract—urination.  
	Low temp on skin, low pH in stomach.
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2
Q

physical barriers: cell derived chemical

A

produced by epithelial cells
 Mucous, perspiration, saliva, tears, earwax. Trap and contain.
 Lysozymes (in swat, tears and saliva) attach cell walls of gram + bacteria
 Fatty acids and lactic acids secreted from sebaceous glands on skin kill bacteria and fungi and create a acidic environment on skin
 Epithelial cells contain antimicrobial peptids
• Defensins—from neutrophils and epithelial cells disrupt bacterial membrane
• Collectin—soluble glycoprotein that facilitate recognition by macrophages

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3
Q

physical barriers: normal microbiome

A

 Produces enzymes that facilitate digestion of large polysaccharids and fatty acids
 Synthesize vitamins (K and B)
 Release ammonia, phenol and indols (toxic to pathogens)
 Competes with pathogens for nutrients and blocks attachment
 Fosters adaptive immunity by inducing growth of gut-associated lymphoid tissue
 Contributes to bidirectional communication between brain and GI tractimplications for cognitive function, behavior, pain modulation, stress responses and disease

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4
Q

Inflammation is characterized by

A
  1. Occurs in vascularized tissue, 2. Rapid response (seconds) 3. Cellular and chemical 4. NONSPECIFIC. Same regardless of injury
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5
Q

acute signs of inflammation

A

rubor (red), calor (heat), tumor (swelling), dolor (pain), function laesa (loss of function)

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6
Q

what happens @ site of injury/inflammation

A

increased coagulation, vasodilation, WBC adhesion, increased vascular permeability, pain

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7
Q

what is lymphangitis and lymphadenitis and why do they occur with acute inflammation?

A

swelling of lymph vessels and lymph nodes due to increased work (draining extravascular fluid to lymph nodes)

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8
Q

benefits of inflammation

A
  • Prevents infection and further damage
  • Limit scope of inflammatory process (clotting, plasma enzymes and blood tissue cells prevent spreading of inflammation to healthy tissue)
  • Preparation of injury for healing and repair (removal of bacterial organisms, dead cells and debris)
  • Facilitates adaptive immunity—antigens+macrophages and lymphocytes concentrated in nodesinitiates adaptive immunity to protect from future exposures.
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9
Q

3 key system of plasma protein systems in innate immunity

A

complement, clotting and kinen

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10
Q

Complement

A

plasma system of innate immunity
complements the capacity of antibodies and phagocytes to clear pathogens and dead cells and activate inflammation
• Consists of complement factors (proteins).

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11
Q

Activation of C3 and C5 results in 3 potent molecules being released, what are they and what do they do?

A
  • C3b—opsonins—coat bacteria
  • C5a—chemotactic—like a magnet attracts leukocytes
  • C3a and C5a together are called anaphylatoxins—degranulates mast cells to release histamine which increases vasodilation and capillary permeability
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12
Q

What is a membrane attack complex (MAC)?

A

• Complements c6-c9. Leads to bacterial destruction and tissue injury by creating pores in outer membranes of cells or bacteria. These cause the infusion of water into the cellscell death

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13
Q

What are the 3 pathways for complement activation?

A

classical, alternative and lectin

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14
Q

describe the classical complement activation system

A

activated by antibody/antigen complexes, or CRP—activate C1 and leads to cascade

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15
Q

describe the alternative complement activation system

A

doesn’t need antibodies. activated directly by substances on the surfaces of infectious microorganisms (lipopolysaccharides/endotoxins on bacteria or zymosan (carbohydrate on yeast cells). Uses factor B, D and properdin to form complex that activates C3 and C5, then converges with classical pathway.

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16
Q

describe the lectin pathway (3rd complement pathway)

A

independent of antibodies. Activated by plasma proteins like mannose-binding lectin (MBL). Binds to bacterial polysacc. That contain mannose (a carm) and activates the complement cascade
(mannose binding lectin)

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17
Q

describe the clotting system in innate immunity

A

plasma proteins form a blood clot. Can be activated by collagen, enzymes and toxins released during tissue injury or infection
• Blood clot consists of mesh of fibrin strands and platelets (primary initiator of clotting).
• Function to plug the vessel and stop bleeding, trap the microorganism and prevent spread.

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18
Q

name the 2 pathways for clotting and describe each

A

intrinsic and extrinsic
• Tissue factor (EXTRINSIC) pathway—activated by TF aka thromboplastin released by damaged endothelial cells of blood vessels. Reacts with activated factor VII
• Contact activation (INTRINSIC) pathway—activated when vessel wall damage causes negatively charged subendothelial subst. to come into contact with factor XII (Hageman factor) in plasma
• BOTH CONVERGE AT FACTOR X
 Activates fibrinfibrin clot activates clotting systemfibrinopeptides which attracts neutrophils (chemotaxis) and increase vascular permeability

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19
Q

What is the kinin system?

A

interacts with clotting system. Clotting AND kinin initiated through activation of Hageman factor (XII) which results in formation of factor XIIa activates prekalikreinkallikreinkininogenbradykinin (final product)
• Bradykinin causes dilation of blood vessels and induces pain, smooth muscle cell contraction and increases vascular permeability

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20
Q

name 6 inhibitors of inflammation

A 
protease inhibitor
carboxypeptidase
kininase
histaminase
fibrinolytic system
plasminogen
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21
Q

define protease inhibitor

A

inhibits activation of complement (inhibits inflammation)

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22
Q

how dose carboxypeptidase stop inflammation

A

inactivates C3a and C5a

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23
Q

kininase

A

degrenates kinins (inhibits inflammation)

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24
Q

histaminase

A

degrades histamin and kallikrein (inhibits inflammation)

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25
Q

fibrinolytic system

A

limits size of clot and degrades clot after bleeding stops

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26
Q

plasminogen

A

plasmin degrades the fibrin polymers in clots

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27
Q

what is the principal coordinator of clotting?

A

vascular endothelium

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28
Q

explain how cell receptros work

A

binding to these results in cell activation aka pattern recognition receptors (PRRs). they monitor for cell damage and infectious agents by recognizing inf. Micro org. and damaged cells in 2 ways
PAMP (pathogen assoc. mol. patterns) and DAMPS (damage associated mol. patterns)

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29
Q

name the cellular components of inflammation

A

mast cells, macrophages and dendritic cells, RBCs, leukocytes (granulocyte, monocyte, lymphocyte)

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30
Q

what does a c-type lectin receptor recognize?

A

fungal antigens

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31
Q

intracellular receptors

A

NLR and NOD (nucleotide binding and nucleotide oligomerization) in lymphocytes, macrophages and dendritic cells.

32
Q

cytokines

A

cell mediators: intercellular signaling molecules secreted by variety of cells to bind to specific cell membrane receptors. regulate innate/adaptive immunity. Can produce systemic effects like fever CAN BE Proinflammatory or antinflammatory

lymphokines, monokines, , chomkines

33
Q

Interleukins function to

A

alter behavior of cells
 Regulate CAM (cell adhesion molecules)
 Regulate Chemotaxis (attraction of leukocytes to inflammation)
 Induction, proliferation and maturation of leukocytes in bone marrow
 Enhance or suppress inflammation and adaptive immune response

34
Q

interleukins are producted by

A

macrophages and lymphocytes

35
Q

Proinflamatory cytokines

A

TNF Alpha and IL1 and IL6

36
Q

TNF Alpha

A

proinflammatory cytokine
interacts with IL1 and IL6
chemotaxis, phagocytosis, inflamm and adaptive immune prolif.
• TNF contributes to damaging effects of chronic inflammation
• Induces fever, increased liver synthesis of inflammation proteins, cachexia and intravascular thrombosis

37
Q

IL1

A

proinflammatory cytokine
produced by macrophagesactivates monocytes, lymphocytes and macrophages
• Endogenous pyrogen (causes fever)

38
Q

IL6

A

proinflammatory cytokine produced by macrophages, lymphocytes and fibroblasts. Induces hepatocytes in liver to produce proteins for inflammation.

39
Q

Anti-inflammatory cytokine

A

IL-10, TGF-Beta

suppress lymphocytes

40
Q

Interferon (IFN)

A

protect against viral infection
type 1 produced/released by infected cell
Type 2 produced by lymphocytes

41
Q

Mast Cells are potent activators of

A

Inflammation

42
Q

mast cells are activated by

A

tissue damage or complement cascade and IgE (allergies)

43
Q

When a mast cell degranulates what is released?

A

release their contents within seconds of stimulus

What’s inside? Histaminesconstriction of smooth muscle and dilation of post capillary venulesincreased blood flow

44
Q

H1

A

histamine binds to this and causes smooth muscle contraction and bronchoconstriction

45
Q

H2

A

histamine binds to this and suppresses leukocyte function,

H2 blockers reduce gastric acidity

46
Q

Mast cells synthesize:

A

mediators: leukotrienes, prostaglandins and platelet activating factor

47
Q

Leukotrienes

A

induce smooth muscle contraction (bronchoconstriction) and increase vascular permeability, stimulate slow, prolonged inflammatory responses (as apposed to rapid acting histamine)

48
Q

prostaglandins

A

increase vascular permeability, neutrophil chemotaxis and pain. Produced by COX
COX-1 activates platelets and protects stomach lining
Cox-02 associated with inflammation

49
Q

platelet activating factor

A

produced by neutrophils, monocytes, endothelial cells, mast cells and platelets. Cause endothelial cell retractionincreased vascular permeability, adhesion of leukocytes and platelet activation (can also activate mast cells

50
Q

How to endothelial cells help in healing/immune attack

A

when injured endothelial cells promote recruitment and invasion of leukocytes
 Histamine and bradykinin stimulate endothelial cell contraction
 Promote angiogenesis and facilitate wound healing

51
Q

platelets

A

aneucleated.

 Can degranulate and release serotonins, similar to histamine.

52
Q

Neutrophils in innate immunity

A

granulocyte with multilobed nucleus
 PREDOMINANT phagocytes in early inflammation
 Primary role to phagocytize microbes and cellular debris.
 Short lived (incapable of division)
 Component of pus

53
Q

eosinophils

A

defend against parasites and in allergies

54
Q

basophils

A

 Basophils—least prevelant granulocyte. Releases histamine, important in aX and asthma

55
Q

dendritic cells

A

phagocytic cells in peripheral organs and skin. Eat them and bring to T lymphocytes (adaptive immunity)

56
Q

lymphocytes and NK cells

A

lymphocytes are a type of WBC and activate macrophages and initiate immune response against pathogens and cancer.

 B lymphocytes produce antibodies
 T lymphocytes reulate immune cells, kill firuses and cancer
 NK cells—type of lymphocyte eliminate virally infected and cancer cells. Have inhibitory and activating receptors bind to cells produce cytokines and kill target cells

57
Q

Cells of phagocytosis

A

neutrophils and macrophages

58
Q

opsonization

A

increases phagocyte adherence. coats the cell with opsonin. C3b and antibodies are good at this

59
Q

describe endocytosis

A

microorganism drawn into phagocyte. Forms a phagocytic vacuole or phagosome. Lysosomes fuse with this and discharge their contents to destroy the organism

60
Q

when phagocytes die what is released to inhibit inflammation associated with tissue damage from enzyme released from dead phagocyte?

A

• Alpha 1 antitrypsin (protease inhibitor) and catalase (breaks down h202) inhibit the destructive effects

61
Q

systemic signs of acute inflammation

A

 Fever—d/t cytokines like TNF and IL1—endogenous pyrogens. Act on hypothalamous
 Leukocytosis—increase in circulating WBCs >11,000
 Left shift (increase in ratio of immature to mature neutrophils)
 Plasma protein synthesis—produced by liver and inc. during inflammation
 Maximal 10-40 hours after onset of inflammation
• Increased fibrinogenincreased ESR )RBCs clumping with fibrinogen)
• CRP increased—produced by liver, esp for autoimmune diseases and severity of inctious disease

62
Q

Chronic inflammation

A

inflammation that lasts >2 weeks
all chronic disease have a component of this.
pus formations, purulent d/c and incomplete wound healing are signs.

63
Q

granuloma

A

in chronic inflammation these can form to block off the area affected.  Causes caseous necrosis or liquefaction necrosis. Fluid eventually gets out and leaves a hollow walled structure (TB)

64
Q

Wound healing with full regeneration (no scar tissue)

A

resolution.

epithelium in skin, liver and intestines

65
Q

4 phases of wound healing

A

hemostasis (coagulation), inflammation, proliferation, remodeling/maturation
 Phase 1: hemostasis (coagulation)

66
Q

Phase 1 of wound healing

A

• Tissue damagebleedingvasoconstriction and vasodilationcoagulation cascade. Fibrin mesh + platelets. Platelets degranulateincreased capillary permeability initiatin proliferation of undamaged cells

67
Q

phase 2 of wound healing

A

inflammation—begins within minutes—macrophages and mast cells release vasoactive cytokinesinc blood flow, neutrophils infiltrate, lymphocytes activate immune response

68
Q

Phase 3 of wound healing

A

: proliferation and new tissue formation—days 3 to 4 lasting-up to 14. Fibrin clot replaced by normal tissue or scar tissue.
• Invasion of macrophages which clear debris and promot collagen synthesis and angiogenesis
• After clean up (debridement) vascular dilation and permeability is reversed preparing for regeneration or repair
• Granulation tissue grows
• Epithelialization occurs
• Fibroblasts—deposit connective tissue.
• Wound contraction occurs

69
Q

phase 4 of wound healing

A

remodeling/maturation
begins several weeks after injury and completed within 2 years. Continuation of cell differentiation, scar formation and remodeling.
 Dysfunctional wound healing

70
Q

Geriatric considerations of immunity

A

chronic disease, prone to overwhelming sepsis, skin loses regenerative ability, medications impair response, infection and inflammation more common

71
Q

Pediatric considerations of immunity

A

decreased inflammatory immune function, neutrophils not as good @ chemotaxis, complement deficiency, decreased oxidation and bactreal response, prone to sepsis.

72
Q

primary immune cells in the tissues

A

macrophages (were monocytes in the blood) and Mast cells

73
Q

name two mediators that increase edema/vascular permeability in acute inflammation

A

histamine (d/t mast cell degranulation) and nitric oxide (produced from endothelium and macrophages) also eicosanoids (leukotrienes and prostaglandins

74
Q

what happens with complement activation

A

after C1 is activated, C1-C4 are activated, result in mast cell degranulation, neutrophil chemotaxis, microbe opsonization, lysis, RBC mediated clearance and B-cell activation

75
Q

What is complement?

A

system of molecules, regulators and receptors in host defence

advance pathophys (6 decks)

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