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Nur 1142 Patho > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What is innate immunity?

A

Natural barriers (physical and biochemical) and inflammation

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2
Q

Surface barriers harbour what?

A

Natural flora (group of microorganisms) that protect against pathogens

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3
Q

What’s the role of the physical and biochemical barrier in innate immunity?

A

It’s the first line of defence at the body surface, in place at birth to prevent damage by substance from environment and thwart infections by pathogenic microorganisms

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4
Q

What is the second line of defence?

A

Inflammatory response

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5
Q

What is the role inflammation response?

A

Inflammatory response is activated to protect against further injury, prevent infection of injured tissues and promote healing

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6
Q

What is adaptive (acquired or specific) immunity?

A

3rd line of defence
Slower
More specific process
Targets particular invading microorganisms and eradicate them
Body develop memory for rapid response at future exposure to the same organism

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7
Q

What is the timing of the first line of defence!

A

Constant

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8
Q

What is the specificity of immunity in first line of defence?

A

Broadly specific

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9
Q

What are the cells involved in first line of defence?

A

Epithelial cells and microbiome

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10
Q

What type of memory occurs in first line of defence in innate immunity

A

No memory involved

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11
Q

What are the active molecules in innate immunity first line of defence?

A

Defensins,
cathelicidins,
collectins,
lactoferins,
bacteria toxins

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12
Q

Protection in the first line of defence in innate immunity involves what?

A
  1. Anatomical barriers( skin and mucus membranes
  2. Cells and secretory molecules ( lysozymes, low pH of stomach and urine)
  3. Ciliary activity
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13
Q

Inflammatory response occur as what?

A

Second line defence response to tissue injury or infection

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14
Q

What type of response do we have in 2nd line defence of innate immunity?

A

Immediate response

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15
Q

What type of specificity of response do we have in 2nd line defence of innate immunity?

A

Broadly specific

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16
Q

What cells are involved in the 2nd line defence of innate immunity?

A

Mast cells
Granulocytes- ( neutrophils, eosinophils, basophils)
Monocytes/macrophages
Natural killer cells (NK)
Platelets
Endothelial cells

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17
Q

What is the type of memory in 2nd line of defence in innate immunity?

A

No memory

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18
Q

What are the active molecules in 2nd line defence of the innate immunity?

A

Compliments
Clotting factors
Kinnins
Cytokines

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19
Q

What is the process involved in 2nd line defence of innate immunity?

A
  1. Vascular response
  2. Cellular component( mast cells, neutrophils, macrophages)
  3. Secretory molecules or cytokines
  4. Activated plasma protein system
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20
Q

What are the 3 lines of human defence from infections and injury

A
  1. Innate immunity (natural barrier)
  2. inflammatory response and
  3. adaptive(acquired) immunity
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21
Q

What are the physical barriers in innate immunity?

A

Skin and mucus membranes

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22
Q

List the antibacterial peptide that provide biochemical barriers against pathogens in mucus secretions, perspiration, saliva, tears and other secretions

A

Cathelicidin
Defensin
Collectins
Mannose binding lectins

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23
Q

What are the functions of commensal and mutualistics organisms that colonize mucus membrane and skin or what are functions of microbiomes

A

Release chemicals that facilitate immune response
Prevent colonization by pathogens
Facilitate digestion in GI tract

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24
Q

What are the characteristics of inflammatory response

A

It’s the 2nd line of defence
It’s rapid and non specific
It can only occur in the vascularized tissue

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25
Q

Where does inflammatory response occur?

A

Vascularized tissues only

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26
Q

What are the macroscopic hall mark of inflammatory response

A

Redness
Swelling
Heat
Pain
Loss of function of the inflamed tissue

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27
Q

What are the microscopic hallmarks of inflammatory response?

A

Vasodilation
Increased capillary permeability
Accumulation of fluid and cells at inflammation site

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28
Q

What are the 3 key plasma protein systems involved in inflammation

A

Complement system
Clotting system
Kinin system

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29
Q

What protein system is bradykinin found

A

Kinin system

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30
Q

What’s the role of bradykinin in inflammation

A

Vascular permeability, smooth muscle contractions and pain

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31
Q

What are the types of cells involved in inflammatory process

A

Mast cells, endothelial cells, platelet, phagocytes(neutrophils, eosinophils, monocytes/macrophages, dendritic cells) natural killer cells and lymphocytes

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32
Q

List the cytokines(biochemical mediators in innate immunity

A

Chemokines
Interleukins
Interferons
Other molecules

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33
Q

What’s the function of interleukin 10?

A

To down regulate inflammatory response

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34
Q

What’s the most important activator of inflammatory response is what?

A

Mast cells

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35
Q

What’s the function of histamine in inflammatory process?

A

Causes capillary dilation and retraction of endothelial cells lining capillaries causing increased vascular permeability

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36
Q

What is interstitial space?

A

Free and opened space between tissue endothelial calls and vasculatures

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37
Q

What is tissue endothelial cells

A

Walls and intercellular space and content e.g nucleus

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38
Q

When mast cells are triggered by damaged endothelial cells or endotoxins what are the immune cytokines released?

A

Histamine
Leucotrienes
Prostaglandins
Chemotatic factors (positive chemotaxis)
TNF (alpha), interleukins (IL, 4, 5, 6, 13)

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39
Q

What are the 2 major area in mast cell reaction!

A

Degranulation and synthesis

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40
Q

Degranulation of mast cell produce 3 reactions

A
  1. Histamine for vascular effect
  2. Cytokines- TNF alpha and interleukim 4, 5, 6, 13 for inflammation
  3. Chemotatic factors to attract neutrophils and eosinophils to start phagocytosis
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41
Q

What is the function of histamine in innate immunity

A
  1. Vasodilation, by rapid constriction of smooth muscles, and dilation of post capillary venules causing increase blood flow to micro circulation
  2. Increase vascular permeability
    Increase adherence of leukocytes to endothelium
  3. Affect binding sites H1 and H2 on target cell surface
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42
Q

What’s the function of chemotatic factors in Degranulation of mast cells

A

Attract neutrophils and eosinophils to start phagocytosis process

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43
Q

What is the function of cytokines in mast cell Degranulation?

A

Cytokines - TNF alpha and IL 4, 5, 6, 13 Tiggers overall inflammation process. Call for phagocytize cells and plasma to manage pathogen and for healing

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44
Q

Mast cell synthesis involves what?

A

Damaged epithelial or tissues has phospholipid on surface which need to be broken down for repair by enzyme - phospholypase A2 which into breaks down arachidonic acid and platelet activating factors.
Arachidonic acid is broken down into 2 enzymes Lopo- oxygenase and cyclo oxygenase. Cyclo-oxygenase produce leukotrienes which has vascular effects and lipooxigynase produce prostaglandin which has vascular effect and pain

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45
Q

Arachidonic acid is broke down into 2 enzymes what are they?

A

Lopo- oxygenase (LPO) and cyclooxygenase (COX1 or COX2)

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46
Q

In mast cell synthesis, Phospholipase A2 breakdown phospholipid to what?

A

Arachidonic acid and platelet activating factors

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47
Q

What is the role of platelet activating factor in mast cell synthesis?

A

1 Vascular effects- Increase vascular permeability by relaxing smooth muscles and creating gaps in the cells lining the internal vasculature
2 platelet activation for clotting

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48
Q

Cyclooxygenase breaks arachidonic acid into what? And what’s the function of the product?

A

Prostaglandin

Function:
Contribute to vascular permeability
Pain
Neutrophil chemotaxis

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49
Q

Lipooxygenase breakdown arachidonic acid into what? And what is the function of the product?

A

Leukotrienes
Function
Vascular effect- leukotrienes impact smooth muscles, and increase vascular permeability by contracting the endothelial cells in similar way to platelet activating factors and histamines

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50
Q

Corticosteroids work by what?

A

Inhibiting phospholipase

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51
Q

NSAIDs mechanism of action is what?

A

Inhibits COX from producing prostaglandin

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52
Q

Mast cell histamines attach to what receptors!

A

H1 rectepor or H2 receptor

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53
Q

What is inflammation?

A

Reaction to tissue damage or invasion by microorganisms

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54
Q

What is the function of inflammation?

A

To manage invading organisms, clean up debris and initiate healing

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55
Q

What are the 4 characteristics of inflammation?

A
  1. It occur in tissues with good blood supply
  2. Vascular response(humoral response)
  3. Activated rapidly within seconds of cellular damage
  4. Include cellular and chemical reactions at vascular and interstitial levels.
    It is non specific and antibodies are not involved at the onset
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56
Q

H1 rector activate what?

A

Smooth muscles cells and epithelial cells

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57
Q

What is the effect of Binding of Histamine to H1 receptor on smooth muscles and endothelial cells?

A

Contraction or vasodilation
Contraction ( retraction at endothelial junctions)

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58
Q

What is the effect of Histamine binding to H1 receptors on neutrophil/mast cells?

A

Neutrophils = Increase chemotaxis Mast cells = prostaglandin synthesis

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59
Q

Binding of Histamine to H1 receptor causes what

A

Cell activation of target cells - smooth muscle cell endothelial cell, neutrophil and mast cell.

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60
Q

Binding of Histamine to H2 receptor causes what?

A

Cell deactivation resulting in decrease leukocytes, eosinophil, neutrophil and mast cell

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61
Q

What is the effect of histamine binding to H2

A

Decrease lymphocyte and eosinophils activity
Decrease neutrophil chemotaxis
Decreased mast cell Degranulation

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62
Q

H1 receptor blockers/antagonist are?

A

Antihistamines used for allergic immune reactions

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63
Q

H2 receptor blockers/antagonist examples are

A

Famotidine (Pepcid)
Ranitidine (Zantac)
They plug H2 receptor causing decrease in gastric acid in stomach lining.
They are used to treat acid reflux and peptic ulcer

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64
Q

What we the plasma protein systems in inflammatory response

A

Complement system
Clotting system
Kinin system

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65
Q

True or false: mast cell reactions takes place same time as plasma protein system reactions

A

True

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66
Q

What’s the other name for Factor XII

A

Hageman factor

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67
Q

In the Kinin system, vascular endothelial damage activate what?

A

Hageman factor (factor XIIa which triggers clotting and Kinin system

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68
Q

What’s function of prekallikrein also known as factor XIIa

A

Activate kinin system

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69
Q

Prekallikrein (Factor XIIa) is used to produce what?

A

Kallikrien and kininogen

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70
Q

Kininogen is a precursor for what?

A

Bradykinin

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71
Q

What is the function of bradykinin

A
  1. Vasodilation
  2. Smooth muscle contraction and increase permeability
  3. Act with prostaglandins to induce pain
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72
Q

Clotting system is triggered by what?

A

Tissue injury/ infection
Collagen
Proteinase
Kallikrein
Plasmin
Bacterial endotoxins

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73
Q

What is the purpose of clotting cascade

A

Plug formation and to stop bleeding
Trap microorganisms and prevent spread
Framework to form repair and healing

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74
Q

In the clotting system of inflammatory response the fibrinopeptide do what?

A

Fibeinopeptides are Chemotatic, migration of neutrophils and
Increase vessel permeability

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75
Q

What is the function of fibrinogen in the inflammatory response?

A

1 Produce fibrin for blood clot
2. Release fibrinopeptides which cause migration of leukocytes(neutrophils) and increase permeability

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76
Q

Fibrinogen can enhance bradykinin formed from Kinin system, true or false

A

True

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77
Q

What are the 2 pathways is clotting cascade?

A

Intrinsic and extrinsic pathways

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78
Q

The extrinsic pathway is triggered by what?

A

Damage to the endothelial cells in the blood vessels triggers Tissue factor(TF) thromboplastin - extrinsic pathway and trigger factor VIIa

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79
Q

What triggers the intrinsic pathway?

A

Damage to the full vessel triggers contact activation( intrinsic pathway) and triggers Hageman factor (factor XII to XIIa or prekallikrein)

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80
Q

Both intrinsic and extrinsic pathway trigger what?

A

Both pathways converge at Factor Xa which is activated in to fibrin that polymerizes into fibrin clot

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81
Q

What does fibrinogen trigger in the clotting cascade

A

Fibrinogen triggers fibrinopeptide, Chemotatic (neutrophil) and vascular permeability and enhance bradykinin formed from Kinin system

82
Q

What is the deference between monocytes and macrophages?

A

They are the same cell.
Inside vasculature it’s called monocytes
When it squeezes through gap and fall into interstitial space, it’s call macrophages

83
Q

What is margination or pavementing?

A

When both leukocytes and endothelial cells begin expressing molecules (selectins and intergrins) that increase adhesion or stickiness causing leukocytes to adhere more avidly to the endothelial cells in the walls of the capillaries or venules

84
Q

What is margination and pavementing?

A

P selectins encourages and captures plasma cells ( specifically WBC/granulocytes) that is needed in interstitial space for repair and cleanup via phagocytosis

85
Q

What are the examples of phagocytic cells

A

Neutrophils, monocytes/macrophages, dendritic cells

86
Q

What is DIAPIDESIS or emigration?

A

Squeeze through endothelial gaps via PECAMs(platelet endothelial cell adhesion molecules) and move into the extra vascular space

87
Q

Chemotaxis or directed migration

A

Once interstitial space key Chemotactic factors signal to neutrophil/macrophages to move towards the area of injury/pathogen to killing/healing

88
Q

What’s the process of heat, erythema, edema and pain observed in inflammatory response

A
  1. Once mast cell (histamine, leukotrienes, prostaglandins), clotting system, kinin system and complement systems are triggered
  2. Smooth muscle relax causing vasodilation and increase blood flow to the area causing (erythema and heat).

3.Epithelial gap allow Permeability which allow plasma fluid (fluid, WBC, RBC etc) to leak into interstitial space = edema & joint immobility.

  1. Increased pressure from fluid in interstitial space applies pressure on the nociceptor (sensory neurons) which activate pain
  2. Bradykinin (kinin system) and prostaglandin (mast cells) triggers the nociocpetor which activates them to produce pain
89
Q

What cause erythema and heat in inflammatory response

A

Relaxation of smooth muscles which results in vasodilation and increase blood flow to the area

90
Q

What causes edema in inflammatory response

A

Endothelial gaps allow permeability which allow plasma ( fluids, WBC, RBC) the leak through the interstitial space

91
Q

What are the 2 ways pain occur in inflammatory response

A
  1. Increase pressure from interstitial space apply pressure to nociceptor which activate them to produce pain
    
  2. Bradykinin (Kinin system) and prostaglandin (mast cell) tiggers, the nociceptor which activate them to produce paint
92
Q

Fever in inflammatory response is caused by what?

A

Cytokines IL1, IL6, TNF alpha, prostaglandin, endogenous pyrogens acts on hypothalamus which produce prostaglandin E2 (PGE2) increase the body temperature to kill pathogens and increase metabolism

93
Q

What the function of Prostaglandin E2 (PGE2)

A

Increase body temperature to kill pathogens and increase metabolism to increase healing

94
Q

Leukocytosis

A

Increase in WBC and left shift ratio of immature neutrophils are more than mature neutrophils due to demand on bone marrow to produce more

95
Q

Systemic manifestation of inflammation - liver

A

Plasma protein synthesis- increased synthesis of plasma protein IL1 and induction of IL6 stimulate the liver cell production of active phase reactant

96
Q

Active phase reactants are what?

A

The are pro/anti inflammatory.
They are produced in the liver by increase synthesis of plasma protein IL1 and induction of IL 6

97
Q

C reactive protein (CRP) is specific for what?

A

Inflammation
CRP is produced in the liver

98
Q

Systemic manifestation of inflammatory response - fibrinogen

A

Fibrinogen is associated with adhesion among erythrocytes and increased sedimentation rate ESR.

ERS is indication for inflammation but non specific for inflammation

99
Q

What are the 2 biggest phagocytes

A

Neutrophils and macrophages

100
Q

Difference between neutrophils and macrophages

A

Neutrophils are members of the WBC (granulocyte)
They arrive early 6-12hrs after initial injury
They are sensitive to acidic environment-short life
Mature cell is unable to divide
Found in purulent exudates
They do not activate the adaptive immune system

101
Q

Macrophage are antigen presenting cells
True or false

A

True

102
Q

Macrophage characteristic in inflammatory response

A

They a monocytes, when they migrate into tissue for inflammation, they are called macrophages

They appear 24hrs to 3-7 days after neutrophils

They are able to divide

They are attracted by macrophage Chemotatic factors released by neutrophils

They play key role in activation of adaptive immunity- they are antigen presenting cells

103
Q

Which are the antigen presenting cells

A

Macrophages and dendritic cells

104
Q

What is left shift?

A

Ratio of immature form of neutrophils such as band cells, metamyelocytes and occasionally myelocytes are present on relatively greater then normal propoetion

105
Q

One of the major link between the innate and acquired immunity is what?

A

Dendritic cells

106
Q

What is the location of dendritic cells

A

Peripheral organs and skin

107
Q

Dendritic cells migrate through lymphatic vessels to where

A

Lymphoid tissues (lymph nodes)

108
Q

Dentritic cells interact with T lymphocytes to generate what?

A

Acquired immunity

109
Q

Function of dendritic cells

A

Primary phagocytize cells - antigen presenting cell

110
Q

Eosinophils function

A
  1. Primary defence against parasites.
    Occurs in collaboration with specific antibodies produced by acquired immune system
  2. Help regulate vascular mediators released from mast cells
  3. They are seen in hypersensitivity
111
Q

Basophils

A

Important sources of the cytokine IL4 which is key regulator of adaptive immune system

112
Q

What are the 5 steps to phagocytosis?

A
  1. Recognition and adhesion to target
    2 pseudopods engulfment ( ingestion or endocytosis)
  2. Formation of phagosome
  3. Fusion of a phagosome with lysosomal hydrolytic enzymes
  4. Destruction occur through O2 dependent or independent mechanism
113
Q

What are the hydrolytic enzymes for phagocytosis

A

Protease
Nuclease
Lipase
Glucosidase

114
Q

Recognition and adherence to target in phagocytosis occurs by what process

A
  1. Pathogens- pattens recognition receptor
  2. Opsonization - tight glue for affinity adherence through antibodies and C3b produced by complement system
115
Q

Complement is activated by which 3 pathways?

A

Classic pathway

Alternate pathway

Lectin pathway

116
Q

What’s the complement classic pathway

A

Antibody binds to C1 and activates C3 and C5

117
Q

Alternate pathway

A

Triggered by Substance in surface is bacteria and fungi then use complexes to trigger complement system.

No need for antibodies

118
Q

Lectin pathway triggered by plasma proteins that recognize carbohydrate patterns on the surface of pathogens (bacteria, virus, protozoa, and fungi,) bind to these polysaccharides to activate the complement system.
Pathogen nothing nothing but alternate pathway, can be identified by Lectin pathway

A

Lectin pathway

119
Q

What is the function of complement C3b

A

Opsionin(C3b) - coat bacteria to increase phagocytosis, neutrophils and macrophages

120
Q

What is the function of C5a

A

Chemotatic C5a- chemotaxis/directional migration

121
Q

What is the function of anaphylotoxin- C3a, C5a?

A

Rapid degranulation of mast cells, vasodilation, and capillary permeability

122
Q

Cell lysis(C5b, C6-9, MAC) activation of these complements components that create pores in the outer membrane of cells/ bacteria, permit, water and cause cell death

A
123
Q

Classical pathway is activated by what!

A

Antigen antibody

124
Q

What triggers the classical pathway

A

C1 activating C3 and C5

125
Q

What triggers the alternate pathway

A

Substances on the surface of the bacterial and fungi

126
Q

Does alternate pathway require antibodies

A

No

127
Q

What triggers the lectin pathway

A

Plasma proteins that recognizes carbohydrates pattern on the pathogens

128
Q

Pathogens not noted by the alternate pathway can be identified by lectin pathway- true or false

A

True

129
Q

What is opsonin

A

Coat bacteria to increase phagocytosis- neutrophils/macrophages

130
Q

What complement is responsible for opsonin

A

C3b

131
Q

Complement that play a role in chemotaxis/directional migration is what?

A

C5a

132
Q

What is anaphylotoxin

A

Fragmentation of C3a and C5a resulting Rapid Degranulation of mast cells

133
Q

What is the result of anaphylotoxin

A

Vasodilation and capillary permeability

134
Q

What complement is responsible for anaphylotoxin

A

C3a and C5a

135
Q

Cell lysis by complement is caused by which complements

A

C5b, C6-9

136
Q

Cytokines responsible for vasodilations

A

Prostaglandin, histamine

137
Q

Cytokines responsible for vascular permeability

A

Histamine, bradykinin leukotrienes

138
Q

Cytokines involved with pain

A

Prostaglandins and bradykinin

139
Q

Fever in inflammatory response is caused by

A

IL1, IL 6 TNF alpha and prostaglandins

140
Q

Antimicrobial peptides are?

A

Cathelicidins,
defensins,
collectins
mannose-binding lectin

141
Q

Chemical barriers in innate immunity are what?

A

Saliva, tears, earwax, sweat, mucus
Antimicrobial peptide

142
Q

Perspiration tears and saliva contain which enzyme that help attack cell wall of gram negative bacteria

A

Lysozyme

143
Q

Sebaceous gland contain —— that kill bacteria and fungi

A

Fatty acids and lactic acid

144
Q

Antimicrobial peptide

A

Cathelicidins- attack bacteria that have cholesterol free cell membranes

Defensin- kill pathogens in GI, respiratory urinary and skin

Collectins

145
Q

What are the 4 xtics of inflammatory response

A

Occur in tissue with blood supply )vascularized)

Activated rapidly within seconds after damage occur

Depend on both cellular and chemical components
Non specific- takes place same way regardless of rule of stimuli

146
Q

What causes erythema and warmth in inflammation

A

Vasodilation and increased blood flow

147
Q

What causes edema in inflammatory response?

A

Increased vascular permeability with leakage is plasma from vessels lead to edema

148
Q

What are the major local changes in the inflammatory response?

A
  1. Vasodilation and increase blood flow(erythema and warmth)
  2. Leakage of plasma proteins (edema)
  3. Leukocyte (neutrophils) move from the vessel into injured site
149
Q

What is the plasma systems?

A

Complement
Clotting
Kinin

150
Q

What are benefits of inflammation?

A

1 prevent infection and further damage by invading orgs
2. Limit and control inflammation process - plasma proteins, plasma enzymes and cell prevent inflammation from affecting other cell
3 interact with adaptive immune response
4 prepare injured area for healing

151
Q

Where are dendritic cells located

A

1 they are primary phagocytes located in peripheral organ and skin

152
Q

Function of dendritic cells

A

Migrate through lymph node to interact with T cells to generate acquired immune response

They guide development of Tcell(helper T cells) and co-ordinate development of functional B and T cells

153
Q

What are the 3 processes of phagocytosis

A
  1. Adhesion and dipedesis
  2. Tissue invasion by chemotaxis
  3. Phagocytosis
154
Q

What is the role/ function of inflammation

A

To manage invading organisms and clean up debris
To initiate repair and healing

155
Q

What is tissue endothelial cells?

A

Walls and intercellular space and content e.g nucleus

156
Q

What is interstitial space?

A

Free and open space between tissue endothelial cell and vasculature

157
Q

Vasculature/capillary space are what?

A

Walls with intravascular space and content e.g plasma, RBC and WBC

158
Q

What are the 2 most important phagocytes

A

Neutrophils

Macrophages

159
Q

In inflammation process what is margination/pavementing

A

Increase adherence of neutrophils to endothelium leading to accumulation along vessels wall is call margination/pavementing

160
Q

Increase adherence of neutrophils to endothelium leading to accumulation along vessels wall is call what?

A

margination/pavementing

161
Q

When the neutrophil exit the blood at site of endothelial retraction is called what?

A

Diapedesis

162
Q

By what means does neutrophil exit blood through site of endothelial retraction?

A

Diapedesis

163
Q

Chemotaxis occur when?

A

Neutrophils detect Chemotatic gradients the rough surface receptors, migrate towards high concentration of the factor and high concentrations of Chemotatic factors at the inflammation site mobilizes the neutrophils

164
Q

Phagocytes trap and engulf bacteria using what?

A

PRRs (pattern recognition receptors)

165
Q

Damaged endothelial cells and:pathogens release what?

A

Endotoxins

166
Q

What’s one of the most important cellular activators of inflammation response?

A

Mast cell activation

167
Q

Which cell probably function like mast cells

A

Basophils

168
Q

Corticosteroids work by what?

A

Inhibiting phospholipases

169
Q

NSAID mechanism of action is what?

A

Inhibit cyclooxygenase from producing prostaglandins

170
Q

Acetaminophen works by what mechanism?

A

Blocks a variant of cyclooxygenase

171
Q

What triggers mast cells

A

Damaged endothelial/ invading pathogens

172
Q

Mast cell Degranulation result in what?

A

Production of
Histamine- vasodilation/contraction of vasculature creating gaps

Cytokines: TNF alpha, IL 4, 5, 6, 13- trigger oval inflammations and call for backup in vasculature

Chemotatic factors- call for neutrophils and eosinophils. Neutrophil start phagocytosis process

173
Q

Role of histamine in inflammatory response

A

Increase vascular permeability

Contraction of smooth muscles

174
Q

Binding of Histamine to H1 receptor results in what?

A

Promote inflammation

175
Q

Binding of neutrophils to H1 receptor

A

Increase neutrophil chemotaxis

176
Q

Effect of histamine on H1

A

Contraction

Cont action (retraction at endothelial junction)

Increased chemotaxis

Prostaglandin synthesis

177
Q

Binding of histamine to H2 cause cell inactivation results in what

A

Decrease lymphocytes and eosinophil activity

Decrease chemitaxis of neutrophil

Decrease Degranulation

178
Q

1st and second generation antihistamine block where?

A

H1 receptors

179
Q

Antacids (
Famotidine- Pepcid
Ranitidine -Zantac block with receptor

A

H2- receptor blockers or antagonist

180
Q

Mast cell synthesis result in what

A

Damaged epithelial/tissues has phospholipid that need to be broken down
Phospholipase A2 cleave arachidonic acid into cyclooxygenase and 5 lipoxygenase and tigger platelet activating factor for clot formation

181
Q

5-lipooxigenase breaks down arachidonic acid into

A

Leukotrienes

182
Q

Cyclooxygenase breaks arachidonic acid down to form

A

Prostaglandins

183
Q

What’s function of protaglandins

A

Increase vascular permeability
Neutrophils chemotaxis
Pain

184
Q

Activation of mast cell result in synthesis of what mediators of inflammation?

A

Leukotrienes
Protaglandins
Platelet activating factor

185
Q

Acetylsalicylic acid(Asprin) and NSAID inhibit what

A

COX1 and COX2
But inhibition-of COX1 cause GI toxicity

Célèbrex or celecoxib selectively inhibit COX2

186
Q

What triggers Kinin system?

A

Damage to vascular endothelial activate Hageman factor Factor 12 to 12a trigger clotting and Kinin system

187
Q

What activate Kinin system?

A

Perikallikinin - factor 12 a

188
Q

Prekallikrein activation of the Kinin system result in what?

A

Formation of kallikrien and kininogen

189
Q

Kininogene activate what?

A

Bradykinin

Function of bradykinin - similar to histamine - increase vascular permeability

Stimulate nerve ending causing pain

190
Q

Factor 12 a produced by clotting system activate what

A

Kinin system

191
Q

Clotting system activation?

A

Extrinsic pathway activated by tissue factor and intrinsic (contact activation) pathway lead to factor 10 and thrombin

Thrombin activate proteolytic enzymes activate fibrinogen to fibrin and fibrinopeptide

Fibrin polymerizes to form clot

Fibrinopeptide which are highly chemotactic factors and increase vascular permeability

192
Q

Extravascular molecule connect to the vascular endothelial trigger granules to create what type of endothelial selectins

A

P selectin and intergrins

193
Q

What are p selectin and intergrins

A

Key receptors on the surface of cells inside the vascular and plasma flow

194
Q

What is the role of the p selectin

A

Encourages and captures plasma cells - WBC/ granulocytes that are needed in the interstitial space for repair and clean up by phagocytosis, this process is called margination/pavementing

195
Q

The process called margination/pavementing

A

Process where P selectins Encourages and captures plasma cells - WBC/ granulocytes that are needed in the interstitial space for repair and clean up by phagocytosis, this process is called margination/pavementing

196
Q

What are the phagocytic cells involved in pavementing/margination

A

Neutrophils, monocytes/marcrophages dendritic cells

197
Q

Diapedesis or emigration is what?

A

Squeezing through the endothelial gaps via PECAMs( platelets endothelial cell adhesion molecules) and move into extra vascular space

198
Q

Chemotaxis or directional migration is what?

A

Chemotatic signalling to neutrophils/macrophages to move towards area of injury/pathogen to kill/ heal

199
Q

Mast cell(histamine, leukotrienes, prostaglandin) clotting, Kinin and complement system triggers what?

A

1 smooth muscle relaxation = vasodilation = increased blood flow to area = erythema and heat

  1. Endothelial gaps= increased permeability which allows (fluid, WBC, RBC red) to lease into interstitial space = edema, joint immobility
  2. Increase pressure from interstitial space on nociceptor = pain
  3. Bradykinin (Kinin system) and postaglandin (mast cell) trigger nociceptor cause pain
200
Q

Fever in inflammatory reaction is caused by what?

A

(Cytokines IL 1, IL6 TNF alpha protaglandins) endogenous pyrogens

Nur 1142 Patho (15 decks)

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