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Pathophysiology > Mod 2 Inflammatory Response > Flashcards

Mod 2 Inflammatory Response Flashcards

1
Q

Innate Defences

A

-Non-specific
-No immunological memory
-Fluids (flushing, tears, saliva, mucous, sweat, gastric acid, urine)
-Barriers (skin, mucous membranes, microbiome)
-Phagocytosis/Apoptosis
-Chemical mediators (histamine, pro inflammatory plasma proteins, cytokines, chemokines)
-Inflammation (redness, heat, swelling, pain, loss of function)
-Fever

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2
Q

Adaptive Defences

A

-Specific
-Long-term immunological memory
-Immune responses
-B cells: plasma cells: antibody mediated humoral responses
T cells: cell mediated: direct cytotoxic attack
-Both immunological memory response

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3
Q

Possible outcomes

A

-Body Defenses successful = Health or Healing
-All Defences overcome = injury or disease

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4
Q

Innate Immunity

A

-Also called natural immunity because you are born with these immune functions although may not be fully functional at birth
-Innate responses to a foreign antigen should be immediate, but they do not provide immunological memory (can become ill from same pathogen again)

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5
Q

Adaptive immunity

A

-Contains both PASSIVE (you receive antibodies from someone else) and ACTIVE (you make the antibodies/T helper cells) branches
- Not fully functional at birth, functional at 2
-Takes time to develop 7-14 days for first exposure, then faster for subsequent exposures because of immunological memory (ie presence of b/t memory cells)

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6
Q

Antibodies

A

-Called immunoglobulin (ig)
-Five classes igA,igD,igE,igG,igM
-Presence of specific antibodies in plasma indicated exposure to specific antigen

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7
Q

What is an antigen?

A

Usually foreign, causes body to respond

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8
Q

What happens if 1st line of defence is intact

A

Nothing, stay healthy, foreign agent can’t enter

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9
Q

What happens if 1st line of defence breached?

A

May get infection, tissue breakdown

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10
Q

What happens if 2nd line of deference is activated

A

Inflammation, plasma protein systems activated (clotting), chemical mediators

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11
Q

Purpose of acute inflammatory response

A

Destroy or wall off, promoting healing
Main chemical mediator is histamine

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12
Q

What activates adaptive immune system (3rd line of defence)

A

Histamine release, when second line of defence fails, when b/t cells respond

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13
Q

At what age is adaptive fully functional and when does it start to wane

A

2, 40

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14
Q

B cell stimulates ___, T cell stimulates ___

A

Plasma cells and antibodies
Cell mediated immunity release of cytotoxins

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15
Q

What happens if innate/adaptive immune defences are not successful

A

Stay sick, death, chronic infection/inflammation

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16
Q

What happens if too much histamine is released

A

Hypersensitivity, allergies

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17
Q

What happens if not enough histamine is released

A

Immunodeficiencies, more likely to get infection, slower wound healing

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18
Q

What is inflammation?

A

-Body’s response to tissue damage/infection
-Occurs at the tissue level
-Inflammatory response is initiated by stromal cells, especially mast cells and fibroblasts in connective tissue
-Also requires microvascular response and a variety of pro inflammatory chemical mediators
-Can be acute or chronic
-Often multifactorial, involving both environmental and genetic factors

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19
Q

Tissues are made up of:

A

Stromal cells, parenchyma cells, and interstitial tissue fluid

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20
Q

How well an injured tissue heals depends on

A

Level of vascularization, and type of parenchyma cells in that tissue (can they regenerate)

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21
Q

5 Signs of Inflammation

A

Redness
Heat
Swelling (edema)
Pain
Loss of function

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22
Q

Swelling (Edema)

A

Increase in amount of interstitial tissue fluid
Ie. fluid between the cells; pressure of the excess tissue fluid may irritate nerve endings eliciting pain

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23
Q

Loss of function

A

Usually due to the pain, especially within a joint, also due to swelling causing decreased range of motion

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24
Q

What is the inflammatory response?

A

-Part of second line of innate immune defence
-Occurs when first line of defence breached
-Non-specific, rapid response of injured tissue to any etiological agent of tissue damage
-3 Components: vascular, cellular, and biochemical (plasma protein) responses to tissue damage

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25
Q

What are the 3 major causes of tissue damage

A

Genetic, congenital, or acquired

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26
Q

Purpose of Inflammatory response

A
  1. Limit further tissue damage
    Destroy or dilute out causative agent
  2. Prevent spread of injurious agent/infection
    To wall off causative agent
  3. Stimulate adaptive immune responses
    If innate inflammatory response not able to destroy causative agent
  4. Begin wound healing process
    To bring nutrients, remove wastes (including cell debris)
    — not all responses need all 4 of these utilized Eg if minimal damage like a paper cut, only need diluting out causative agent and nutrient/waste exchange necessary
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27
Q

Role of stromal and parenchyma tissues

A

Both tissues respond to tissue damage

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28
Q

Stromal tissues

A

Microvasculature: arterioles, capillaries, venules
. Endothelial cells increase vascular permeability
. Vascular smooth muscle cells vasodilate
Connective tissues:
. Supportive, binding tissues Eg areolar CT
. Fibroblasts secrete protein fibres collagen
. Mast cells secrete histamine and heparin
- stromal response to injury triggers the inflammatory response with pro inflammatory chemical mediator histamine

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29
Q

Parenchyma tissue

A

The functional cells of the tissue
May be injured and need to heal or be replaced
Do not directly cause the inflammatory response, simply trying to survive and if possible replace cells that have died

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30
Q

Microvasculature

A

-Consists of microscopic blood vessels: arterioles, capillaries, and venules
-All lined with endothelial cells
-Arterioles and venules contain smooth muscles in their walls
-Capillaries are simple tubules of endothelium
-All surrounded by connective tissue
-all have different roles in inflammatory response

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31
Q

Connective tissues

A

-Supportive, binding tissues
-Areolar CT most common type of CT found in every body organ, directly below covering or lining cells called epithelial cells
-Two main types of stromal cells in CT involved with inflammatory response are fibroblasts and mast cells

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32
Q

Fibroblasts

A

-secrete proteinaceous fibers that help form the structural framework of all connective tissues (collagen, elastin and reticulin)

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33
Q

Collagen

A

-Important CT fibre involved in inflammatory response and wound healing
-Helps to stabilize and form the structural framework of the wound site during wound healing
-Also helps trigger blood clotting (coagulation) by interacting with platelets
-Clotting necessary if blood vessels are damaged and the individual is bleeding

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34
Q

Mast cells

A

-Tissue WBC that secrete histamine during the inflammatory response
-Along with basophils also secrete heparin to help prevent unwanted blood clotting within uninjured tissues and the blood stream

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35
Q

Histamine

A

-Potent arteriole vasodilator
-Increases blood flow into the injured tissue
-Basophils in the blood stream can also secrete histamine, important if tissue damage occurs to the inside of a blood vessel

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36
Q

If parenchyma cells cannot be replaced

A

If cannot be replaced by mitosis, tissue/organ deficits may occur

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37
Q

2 types of parenchyma cells that cannot undergo mitosis

A

Heart cardiac cells
Neurons

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38
Q

2 patterns of inflammatory response based on:

A

The duration of response
The specific WBCs present in the lesion
1. Acute inflammatory response
2. Chronic inflammatory response

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39
Q

Acute Inflammation

A

-Innate, immediate tissue response to injury
-Main chemical mediator: Histamine
-Tries to limit the damage and prevent scarring
-Promotes wound healing by bringing in nutrients and removing debris
-Predominant immune cells: Mast cells, neutrophils, macrophages

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40
Q

Chronic Inflammation

A

-Innate and adaptive, prolonged tissue reaction to continued injury or persistent infection
-Main chemical mediator: histamine
-Still trying to limit the damage and promote would healing, but scarring probable
-Predominate immune cells: macrophages, lymphocytes, and mast cells

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41
Q

Neutrophils

A

-Known as first responders
-Can detect low levels of distress signals (Chemicals released by damaged cells and microbes)
-Arrive within hours of injury
-Try to phagocytize debris and pathogens, but are often destroyed by the pathogen

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42
Q

Macrophages (M1)

A

-A few reside within all normal, healthy connective tissue
-However once inflammatory response is triggered, chemicals released by microbes, damaged body cells, and dead and dying neutrophils stimulate a massive influx of new monocytes into injury site
-Monocytes quickly undergo morphological change to become macrophages (M2)

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43
Q

Macrophages (M2)

A

-Commonly known as the “clean up” cells
-Show up a bit later in acute inflammatory response and promote wound healing
-Stick around and work with the lymphocytes if the wound site becomes a chronic issue

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44
Q

Acutely inflamed tissue has

A

Lots of neutrophils, a few M1 —> M2 (dependent on extent of injury)

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45
Q

Chronically inflamed tissue

A

Some M1 —> lots of M2 + lots of lymphocytes (combination of dendritic cells, NK cells, and T lymphocytes
-Within chronically inflamed site, will see aspects of acute and chronic inflammatory responses to the persistent causative agent of injury
-Pathologist would be able to determine specifics by recognizing the WBC’s in tissue sample
-Mast cell numbers will fluctuate based on acuity of reinjury

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46
Q

“Repair” implies

A

-Scar tissue has been produced
-in wound healing, regeneration and resolution are the preferred outcomes
-Hallmark of chronically inflamed tissues is scarring

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47
Q

Characteristics of acute inflammatory response

A

-Begins within seconds
-Innate, non-specific, no immunological memory
-Includes 3 proinflammatory responses to tissue damage

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48
Q

Acute inflammatory benefits

A

Used to prevent spread of infection, bring in nutrients and remove wastes, limit further tissue damage and promote wound healing

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49
Q

Acute 3 pro-inflammatory responses to tissue damage

A
  1. Vascular (microvascular) responses
    -mediated by histamine —> promote vasodilation and increase vascular permeability
  2. Cellular responses
    -mediated by WBCs
    -may include platelets, rbcs, and fibroblasts
    -major WBCs involved: mast cells (secrete histamine) neutrophils, macrophages (clean up cellular debris)
  3. Plasma protein systems responses 3 types: complement, coagulation, and kinin cascades —> promote inflammation, blood clotting
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50
Q

Pro inflammatory plasma proteins acute phase proteins

A

-Most are made in the liver and/or injured tissues
-They circulate at at a low level in the blood plasma as inactive enzymes
-When inactive proinflammatory mediators enter the injury site, they become active enzymes that catalyze different aspects of the inflammatory response
-Operate in a cascade or domino effect
-In response to calls for help from the injured tissues, the liver increase production

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51
Q

3 Major components of acute inflammatory response

A
  1. The vascular response
  2. The cellular response
  3. The plasma protein systems response
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52
Q

The inflammatory response begins with…

A

-The release of histamine from granules stored within tissue mast cells
-Release of histamine is known as MAST CELL DEGRANULATION
-Once released, histamine can trigger all 3 components of acute inflammatory response

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53
Q

The Vascular Response

A

-Immediate histamine-mediated response by the microvascular endothelial and smooth muscle cells within wound site
-Will increase blood flow into the injured tissue and increase vascular permeability

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54
Q

The Cellular Response

A

-Includes all 3 types of blood cells (wbc, rbc, platelets) as they respond to injured tissues distress signals

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55
Q

The Plasma Protein Systems Response

A

-Includes a variety of biochemical responses to injury
-Proinflammatory proteins are part of acute phase proteins
-Transported in blood plasma to injury site to act as proinflammatory mediators

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56
Q

3 Cascades of Plasma Proteins

A

-Interrelated functions
-Complement system
-Coagulation (clotting) system
-Kinin system (weak histamine like effects, elicits pain)

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57
Q

Entire response depends on the chemical mediator ___ released by local tissue ____ cells

A

Histamine, mast cells

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58
Q

Mast cells are located in ..

A

CT surrounding the microvasculature

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59
Q

Histamine receptors are located on..

A

Endothelial cells
Smooth muscle cells

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60
Q

Unlike larger arteries and veins, microvasculature of an organ can..

A

Be increased or decreased depending on organs need, becomes more extensive the more fit you are

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61
Q

Tissue damage stimulates mast cells to..

A

-Rapidly degranulate which releases histamine from storage in cytoplasmic vesicles
-Histamine binds to histamine receptor on vascular endothelial and smooth muscle cells causing specific INDEPENDENT responses

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62
Q

Effects of Histamine on Microvasculature

A
  1. Arteriolar and precapillary sphincter smooth muscle cells —> histamine stimulates vascular smooth muscle cells to relax —> arteriole vasodilation + opens (relaxes) precapillary sphincters —> increased rate of blood flow into capillary bed
  2. Venular endothelium (minor effect on capillaries) —> histamine stimulates endothelial cells to contract —> myoendothelial contraction creates inter-endothelial cell gaps —> increased vascular permeability
  3. Venular endothelium —> histamine also stimulates endothelial cells to decrease production of anti-endothelial adhesion proteins —> allows WBC’s, platelets, and/or rbc’s to squeeze between endothelial cells and infiltrate wound site —> promotes leukocyte infiltration and clot formation
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63
Q

2 Smooth muscle vascular damage effects

A
  1. Arteriolar vasospasm
    -Immediate but brief vasospasm as smooth muscle contracts in response to sympathetic NS release of epinephrine (transient vasoconstriction stress response to injury)
    -Followed quickly within seconds by arteriolar vasodilation (smooth muscle relaxes)
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64
Q

Mast cells

A

-Innate tissue immune cells that recognize and respond to tissue “distress” signals by secreting histamine and other proinflammatory mediators including heparin

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65
Q

Mast cell characteristics

A

-Derived from pluripotent stem cells in red bone marrow
-Reside in connective tissues
-Stromal immune surveillance cells
-Related to basophils, same jobs but reside in different places
-Recognize tissue damage, microbial invasion

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66
Q

How mast cells recognize tissue damage

A

Have lots of cell surface receptors that can bind to a variety of foreign antigen or injured body cell chemical distress signals
Ag receptor binding —> triggers mast cell activation —> histamine secretion

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67
Q

Histamine is a

A

Proinflammatory protein

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68
Q

Heparin

A

-Secreted by mast cells and basophils
-Anticoagulant
-Basophils secrete into bloodstream, Mast cells secrete into stromal connective tissue
-When secreted into bloodstream, prevents platelets from spontaneously aggregating together forming a intravascular thrombus
-When secreted in stromal tissues, helps with dissolution (break down) of a clot as a wound heals

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69
Q

Mast cells vs basophils

A

-Both derived from same red bone marrow stem cells called pluripotent stem cells
-Have similar functions
-Located in two different places
-Mast cells leave the blood stream to reside in tissues (Eg CT, dermis)
-Basophils remain in bloodstream (<1% of peripheral blood wbcs)

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70
Q

Immune cell receptors

A

PRRs
PAMPs
DAMPs
TLRs
Binding of these chemicals to any of these receptors triggers mast cell to respond

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71
Q

Pattern recognition receptors (PRRs)

A

Recognize/bind microbial cell surface chemical patterns

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72
Q

Pattern associated molecular patterns (PAMPs)

A

Recognize/bind products of microbes

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73
Q

Damage associated molecular patterns (DAMPs)

A

Recognize/bind products of body cellular damage (your body’s own distress signals)

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74
Q

Till like receptors (TLRs)

A

Recognize/bind to a variety of microbial cell wall or surface chemicals

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75
Q

Mast cells release proinflammatory mediators by 2 mechanism

A
  1. Mast cell degranulation
  2. Mast cell synthesis
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76
Q

Mast cell degranulation

A

-immediate release of proinflammatory mediators
-mediators made in advance and stored in vesicles within mast cells (look granular)
-releases histamine (elicits all 5 signs of inflammation) that stimulates vascular, cellular and plasma protein responses
-releases chemotactic factors (named for wbc they attract
-releases cytokines (interleukins, tumor necrosis factors)
-

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77
Q

Mast cell synthesis

A

-Slower release of newly synthesized mediators by activated, often injured mast cells within site of tissue damage “distress signals”
-Includes cell membrane components of damaged mast cells —> solubilized (dissolve) in tissue fluids —> signal other wbcs to area of damage
-chemokines - leukotrienes, prostaglandins, & platelet activating factor

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78
Q

What is most potent proinflammatory mediator

A

Histamine

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79
Q

Liver makes

A

Most of the plasma protein system mediators

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80
Q

Chemotactic factor

A

Help stimulate specific types of WBC’s to the area of tissue damage
Includes: neutrophil chemotactic factor, eosinophil chemotactic factor

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81
Q

Cytokines

A

Are communication signals between wbcs, allow them to alert each other to problems “cross talk”
Include: interleukins (ILs) and Necrosis factor (TNF)

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82
Q

Chemokines

A

Chemicals involved in inflammatory response that help wbcs migrate to site of tissue damage
Type of distress signal released by mast cells and other damaged cells in injury site
Include actual components of the damaged cells Eg normal cell membrane components that are released into tissue fluid as a cell dies “hence distress signals”
Include: leukotrienes, prostaglandins, and platelet activating factor

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83
Q

Histamine does not directly cause

A

Pain
However because it stimulates edema that pushes on nerve endings causing them to be compressed or irritated, it is said to elicit all 5 even though one is indirect

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84
Q

I’m response to tissue damage mast cells produce and release a lot of different proinflammatory mediators by 2 processes:

A

Degranulation
Synthesis

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85
Q

Proinflammatory mediators that are made by mast cells in advance and stored in secretory granules are quickly released by

A

Degranulation

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86
Q

Proinflammatory mediators released by degranulation

A

Histamine, chemotactic factor, cytokines

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87
Q

Proinflammatory mediators that are made by mast cells in direct response to injury are called:

A

Newly synthesized

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88
Q

Newly synthesized made from

A

Mast cell cell membrane protein (enzyme) called phospholipase A2 as the mast cell becomes activated

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89
Q

Synthesized Proinflammatory mediators

A

Prostagladins
Leukotrienes
Platelet activating factor

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90
Q

Biochemistry of mast cell synthesis pathways derived from:

A

Phospholipase A2
When released from mast cells cell membrane, becomes soluable (dissolves in tissue fluid) Proinflammatory enzyme that quickly stimulates production of several other Proinflammatory chemicals

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91
Q

Degranulation pathway

A

Mast cell —> Histamine (vascular effects)/Cytokines (inflammation)/Chemotactic factors —> Neutrophil chemotactic factors (attracts neutrophils)/Eosinophil chemotactic factor (attracts eosinophils)

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92
Q

Mast cell synthesis pathway

A

Mast cell —> phospholipase A2 —> platelet activating factor (vascular effects, platelet activation)/Arachidonic acid —> Cyclooxygenase/5-Lipoxygenase —> prostaglandins (vascular effect, pain)/leukotrienes (vascular effects)

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93
Q

Histamine is a

A

Proinflammatory vasoactive amine
Affects microvasculature and other target tissues

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94
Q

Histamine binds to

A

Histamine receptors located on cell membrane of specific target cells
Effects vary depending on specific target cell and subtype of histamine receptors

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95
Q

2 types of histamine receptors

A

H1, H2

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96
Q

H1 receptors

A

Proinflammatory effects on target cells:
Endothelial cells
Vascular smooth muscle
Bronchiole smooth muscle
Immune cells (WBCs)
Most common type

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97
Q

H2 receptors

A

Antiinflammatory effects on target cells:
Gastric parietal (HCI secreting) cells
Immune cells (WBCs)

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98
Q

Although histamine is considered a major Proinflammatory mediator is has some ..

A

Anti inflammatory effects depending on which type of histamine receptors it binds, h1 or h2

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99
Q

H1 endothelial

A

Histamine H1 receptor binding on vascular endothelial cells —> changes gene expression —> actin (contractile/motility protein) produced —> stimulates endothelial cell contraction —> creates small gaps between endothelial cells —> increase vascular permeability; lots on venular endothelial cells

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100
Q

H1 vascular smooth muscle cells

A

H1 rectory or binding on vascular smooth muscle cells —> stimulates smooth muscle relaxation —> arteriole vasodilation; lots on arteriole smooth muscle cells

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101
Q

H1 bronchiole smooth muscle cells

A

H1 receptor binding on bronchiole smooth muscle cells —> stimulates bronchiole smooth muscle contraction —> bronchiole constriction —> decreased gas exchange
Occurs in asthma, anaphylaxis

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102
Q

H1 neutrophils and mast cells

A

H1 receptor binding on neutrophils and mast cells —> promotes neutrophil infiltration and mast cell prostaglandin synthesis
Both are Proinflammatory

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103
Q

H2 gastric parietal cells

A

H2 receptors binding on gastric parietal cells —> stimulates increased gastric acid secretion —> needed for protein denaturation (digestion) but has added benefit of denature glucose microbial proteins in the food we eat; hence anti inflammatory

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104
Q

H2 WBC’s

A

H2 receptor binding on WBCs —> decreases inflammatory response; part of the anti inflammatory events that occur as wound healing begins
Note: many immune cells have both H1/H2 receptors (they can switch type)

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105
Q

H1/H2 receptor switching

A

Depending on where the tissue is within the continuum from acute injury to wound healing, target cells can switch the number of h1 or h2 receptors on their outer cell membrane
Eg. Some WBCs switch from Proinflammatory H1 receptions during inflammatory response to H2 receptors as the inflammatory response wands and wound healing progresses
Other cell types only have one type of histamine receptor Eg, gastric parietal cells

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106
Q

Antihistamines are

A

H1 receptor antagonists

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107
Q

H2 secretion on gastric acid

A

Lymphocyte = decreased activity
Eosinophils = decreased activity
Neutrophils = decreased chemotaxis
Mast cell = decreased degranulation

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108
Q

Effects of histamine on smooth muscle depends on

A

Target organ
In microvasculature—> vascular smooth muscle relaxation —> vasodilation = redness + heat
In bronchioles —> smooth muscle contraction —> bronchiole construction

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109
Q

Anti inflammatory drugs

A

Antihistamines, glucocorticoids, NSAIDS
All have different pharmacokinetics

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110
Q

If mast cell is destroyed

A

Then lots of phospholipase A2 would be released.
Quickly metabolized into arachidonic acid and platelet activating factor

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111
Q

Prostaglandins and leukotrienes

A

Both Proinflammatory distress signals noted by many immune cells

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112
Q

NSAIDS

A

-non-steroidal anti-inflammatory drugs
-include aspirin (ASA, acetylsalicylic acid) and ibuprofen

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113
Q

NSAIDS ASA pathway

A

-ASA blocks the arachidonic acid —> cyclooxygenase (COX) pathway thus has 1) anti inflammatory effects —> decreases vascular effects including pain and swelling and 2) decreases pain signals —> analgesic effects
-ASA also blocks thromboxane A2 which is a pro-coagulant chemical released by activated platelets that promotes platelet plug formation = ASA is also an anticoagulant
-Other NSAIDS block the cyclooxygenase pathway = production of prostaglandins is decreased which decreased vasodilation and vascular permeability —> anti inflammatory effects that decrease
Acetaminophen only block the pain component of the cyclooxygenase pathway —> PG synthesis pathway thus does not have anti inflammatory effects

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114
Q

Corticosteroids/glucocorticoids

A

-Steroidal drugs (aka prednisone, cortisone, hydroxycortisone) and the hormone cortisol made by adrenal cortex that block the release of phospholipase A2
-By blocking PLA2 release, cortisol prevents the production of both the COX and LOX pathways thus blocking prostaglandins and leukotrienes making it a potent anti inflammatory
-Glucocorticoids also block histamine release

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115
Q

Antihistamines

A

Histamine antagonists that block histamine binding to H1 receptors = they also decrease vascular and bronchiole inflammatory responses

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116
Q

Cortisol

A

Major mediator of the stress response that affects both innate and adaptive immune function

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117
Q

Summary Proinflammatory blockage

A

Antihistamines/glucocorticoids = block histamine and vascular effects
Glucocorticoids = block phospholipase A2 production
ASA =block cyclooxygenase
NSAIDS = block cyclooxygenase pathway/prostaglandins

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118
Q

Endothelial responses to histamine stimulation

A

Location: venules and capillaries (minor role)
Histamine receptor: H1
Physiological effects: 1) increased actin gene expression —> increased actin production (contractile/motility protein) —> myoendothelial cell contraction —> inter endothelial cell gaps —> increased local vascular permeability —> edema, pain, loss of function + WBC infiltration and:
2) decreased endothelial cell anti adhesion gene expression —> blood cells adhere to endothelium —> WBC infiltration + platelet adhesion —> platelet activation —> coagulation (clotting)

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119
Q

Vascular smooth muscle response to histamine stimulation

A

Location: arterioles & precapillary sphincters
Histamine receptor: H1
Physiological effect:
Histamine H1 receptor binding —> vascular smooth muscle relaxation —> arteriole vasodilation and precapillary sphincters open —> increased local blood flow into capillary bed —> redness and heat

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120
Q

Histamine-mediated physiological effects via H1 receptor

A

Binding causes Proinflammatory effects of the microvasculature, usually local to the wound site

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121
Q

Systemic vascular Proinflammatory repose

A

Can occur and may be life threatening due to changes in BP, HR, and blood volume (massive systemic arteriole vasodilation), peripheral (including laryngeal) edema, and bronchiole constriction =serious effects of an anaphylactic reaction to an allergen

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122
Q

ARTERIOLE microvascular response to histamine H1 receptor binding

A

Smooth muscle relaxes —> arterioles vasodilate —> increased lumen size —> increased local blood flow —> redness and heat
Occurs mainly on arteriole smooth muscle cells because these smooth muscle cells have the most H1 receptors

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123
Q

PRECAPILLARY SPHINCTERS response to histamine H1 receptor binding

A

Smooth muscle relaxes to open sphincter —> increased lumen size —> increased blood flow into capillary bed —> redness and heat

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124
Q

VENULES response to histamine H1 receptor binding

A

Actin gene expressed —> myoendothelial cell contraction —> interendothelial gaps allow fluid to leave plasma and enter tissues —> increased vascular permeability —> increased local tissue fluid volume —> edema + WBC infiltration into wound site + increased platelet adhesion to endothelium leading to potential coagulation (clotting) cascade, if the blood vessels are damaged
Occurs mainly in venule endothelium because these endothelial cells have the most H1 receptors

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125
Q

CAPILLARIES response to histamine H1 receptor binding

A

Only endothelial cells, no smooth muscle
Can passively expand a bit as increased blood flow from arteriole increases pressure in the capillaries; some myoendothelial cell contraction —> increased vascular permeability

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126
Q

Endothelial cell contraction mechanism via actin

A

-Histamine binding to H1 receptors stimulates endothelial cells to change their normal gene expression and produce a bit of the protein actin
-Once produced actin stimulates the cells to retract their cell membranes allowing microscopic gaps to form between the cells
-Plasma components and WBC’s can leak out of these interendothelial gaps into surrounding tissue fluid, actin will play a role in wound healing
-Histamine also allows all blood cells to come in contact with the endothelium, Will allow phagocytic WBCs to infiltrate the wound site and also promote platelet activation to stimulate coagulation if the tissue damage included injury to the blood vessels, blood clot needed to stop the bleeding
-Healthy endothelial cells express anti adhesion proteins on their outer surface to help prevent blood cells from sticking to them and blocking blood flow. During inflammatory response WBCs need to be able to infiltrate the wound site and platelets which help RBCs need to be able to plug holes in the blood vessel wall. All blood cell types need to be able to adhere to the endothelium, thus the local endothelial cells stop expressing anti adhesion proteins allowing the blood cells to adhere

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127
Q

Blood flow in normal uninjured blood vessel

A

-Axial streaming of blood cells
-Plasma in the plasmatic zone
-Minimal gaps between endothelial cells
-Endothelial cells secrete anti-adhesion chemicals

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128
Q

Blood flow in acutely inflamed blood vessels

A

-Histamine mediated myoendothelial cell contraction —> interendothelial cell gaps lead to
-Increased vascular permeability
-Endothelial cell secretion of pro-adhesion chemicals (CAMS)
-Blood cells enter plasmatic zone —> adhere to endothelium —> enter wound site

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129
Q

Normal blood flow physiology

A

-Normal blood flow is smooth, laminar flow that allows blood cells to travel in the central (axial) zone of the blood stream called axial streaming and lubricating plasma to flow against the endothelial walls of the vessel in the plasmatic zone
-Axial streaming keeps blood cells away from the endothelial cells

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130
Q

Normal blood flow: Plasma

A

Plasma has lubricating effect that prevents too much contact between the potentially sticky blood cells and the endothelial cells lining the blood vessel wall
This lubricating effect prevents unintentional blood cell adherence to vessel endothelial cell walls
Healthy endothelial cells secrete anti adherence chemicals that help prevent all types of blood cells from adhering to them

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131
Q

If platelets bind to the endothelial cells

A

They could adhere and trigger a coagulation (clotting) cascade
Plasma lubrication and anti-adherence chemicals help prevent platelet adherence and possible intravascular blood clotting (thrombus formation)

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132
Q

Interendothelial gaps

A

Allow the vessel to become more permeable allowing intravascular fluid (plasma) and WBCs to shift from intravascular to extra vascular (tissue) compartments
These endothelial cells also stop producing anti adherence chemicals and may even start secreting chemicals that promote platelet and WBC adhesion to the blood vessel wall
WBC adhesion important step in leukocyte infiltration into a wound site

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133
Q

Result of histamine changes in endothelial cell function

A

Increased tissue fluid in wound site; edema + increased WBC infiltration; phagocytosis for wound healing

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134
Q

Venules and histamine endothelial cell function

A

Venule endothelial cells gave lots of H1 receptors and are particularly sensitive to histamine
Venules are considered the major vessels involved in the increased vascular permeability at wound site

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135
Q

Myoendothelial contraction response

A

Very rapid, lasting 15-30 mins post injury

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136
Q

Transient arteriole vasospasm/vasoconstriction

A

Is a stress response to tissue damage
When histamine is released, the arteriole smooth muscle will switch to vasdilation

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137
Q

Summary of Microvascular Response to Histamine

A

Tissue injury —> local tissue mast cells (degranulate and secrete) —> Histamine (binds to H1 histamine receptors on endothelial cells and vascular smooth muscle cells) —> Local microvascular responses —> 5 signs of inflammation

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138
Q

5 cardinal signs of inflammation due to

A

Histamine induced microvascular endothelial and smooth muscle responses to tissue damage

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139
Q

1) Local vasodilation at site of tissue damage

A

-Occurs as smooth muscle relaxes allowing arterioles to vasodilate and precapillary sphincters open
-Local increased arteriole blood flow and increased blood hydrostatic pressure promotes passive capillary dilation within the wound site

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140
Q

Benefits of local vasodilation at site of tissue damage

A

increased blood flow to the injured tissues —> increases nutrients and Proinflammatory mediators delivery to injured tissues, dilutes out causative agent, helps promote water removal and wound healing

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141
Q

Physiological signs of local vasodilation at site of tissue damage

A

Redness, heat

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142
Q

Local increased vascular permeability

A

-Occurs primarily in venules (minor effect on capillaries) —> actin —> endothelial cells contract aka become myoendothelial cells —> creates interendothelial cell gaps —> increases vascular permeability —> allows intravascular fluid (ie plasma) to enter damaged tissue resulting in increased interstitial (tissue) fluid volume

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143
Q

Benefits Local Increased Vascular Permeability

A

Promotes movement of nutrients, WBCs, antibodies, and other proinflammatory mediators out of the blood plasma and into the wound site AND allows wbcs to infiltrate wound site to remove dead and damaged cells and pathogens from the site, promotes blood clot formation (if necessary) and promotes wound healing

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144
Q

Physiological signs Local increased vascular permeability

A

Edema, pain, possible loss of function

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145
Q

What two types of microvascular cells respond to histamine ?

A

Endothelial and smooth muscle cells

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146
Q

What are the effects on the microvasculature in arterioles

A

Vasodilation

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147
Q

What are the effects on the microvasculature in capillaries

A

Passive vasodilation slight stretch

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148
Q

What are the effects of histamine on microvascularture venules

A

Constriction of endothelial cells =increased permeability

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149
Q

Why is the vascular response important during acute inflammation

A

Brings nutrients and WBC’s, proteins to damaged tissues

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150
Q

____ and ____ due to local arteriole vasodilation

A

Heat and redness

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151
Q

____ due to increased local venule permeability causing excess tissue fluid accumulation

A

Edema

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152
Q

___ and ___ due to pressure of the excess tissue fluid pushing on nerve endings and/or if pain inducing chemicals irritating local nerve endings

A

Pain and loss of function

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153
Q

Edema is normally not visible within a tissue until a minimum of __% excess tissue fluid is present

A

30

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154
Q

Edema definition

A

Defined as the excessive accumulation of fluid within the interstitial (tissue) spaces

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155
Q

A tissue with excess tissue fluid is called

A

Edematous

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156
Q

What is third spacing ?

A

Intravascular fluid has gone into the tissue = swelling = generalized Edema

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157
Q

What is ascites?

A

Abdominal fluid accumulation
Liver disease due to protein deficiency

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158
Q

Types of edematous fluid

A

Transudate
Exudate (2 subtypes, fluid exudate, cellular exudate)

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159
Q

Capillary Exchange

A

The movement of fluid between blood plasma and interstitium by filtration or reabsorption

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160
Q

The 2 pressures that promote filtration

A

-Blood/Capillary Hydrostatic Pressure (BHP)
-Interstitial Fluid Osmotic (Oncotic) Pressure (IFOP)

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161
Q

2 Pressures That Promote Reabsorption

A

-Blood/Capillary Colloid Osmotic (Oncotic) Pressure (BCOP)
-Interstitial Fluid Hydrostatic Pressure (IFHP)

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162
Q

4 Body Fluid Compartments

A

-3 are extracellular including 1) blood plasma 2) interstitial fluid 3) lymph
-4th is the intracellular compartment
-Fluid (water + solutes dissolved in the water) is constantly moving between these compartments because nutrients and waste exchange is a constant process

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163
Q

Osmotic Pressure

A

-The pressure exerted by chemicals (especially proteins or sodium) found in a solution that pull/attract water towards them
-i.e they promote osmosis (movement of water from high water area to lower water area) through a membrane
-Osmotic pressure does not require a living/biological membrane to occur

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164
Q

Oncotic Pressure

A

-Is the osmotic pressure exerted by colloids (proteins) in a biological solution, such as blood plasma or interstitial fluid
-If discussing water/fluid movement from one compartment to another within a living body, Oncotic pressure is more direct but both terms are used interchangeably

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165
Q

Fluid filtration

A

2 pressures promote
Filtration of substances (water, nutrients) from blood plasma (I.e. intravascular) into tissue fluid (and then into the body cells)

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166
Q

Reabsorption

A

2 pressures promote
Reabsorption of substances from the tissue fluid (water, cellular waste products, cellular secretions) into the blood plasma

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167
Q

Blood/Capillary Hydrostatic Pressure (BHP)

A

-Promotes filtration
-Water P created by your blood pressure
-Pushes fluid into tissues, allows nutrients to enter tissues

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168
Q

Blood Colloid Osmotic/Oncotic Pressure (BCOP)

A

-Promotes Reabsorption
-Proteins and ions (especially albumin and sodium) that exert osmotic P and pull fluid back into the blood
-Normally helps prevent excess fluid build up in the tissues

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169
Q

Interstitial Fluid Hydrostatic Pressure (IFHP)

A

-Promotes Reabsorption
-Water P that is usually minimal but can increase dramatically during inflammation (due to edema)

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170
Q

Interstitial Fluid Osmotic/Oncotic Pressure (IFOP)

A

-Promotes filtration
-defined as the osmotic P exerted by colloids in interstitial fluid
-usually minimal but if increased, the extra interstitial proteins exert osmotic P and pull water towards them, thus promotes increased tissue fluid (edema)

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171
Q

Intracellular Osmotic P

A

-Normally equal to interstitial osmotic P, therefore cells retain normal morphology

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172
Q

In Healthy Tissue Capillary Exchange

A

-More fluid is filtered than is reabsorbed
-The excess tissue fluid is quickly drained away by the lymphatic system capillaries (about 3L/day)
-No edema occurs
-Normal role of the lymphatic system is to pick up excess tissue fluid and return that fluid (called lymph) to the blood stream

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173
Q

Why are these 4 pressures important?

A

-When arterioles vasodilate and the capillary and venule endothelial cells increase their permeability THEY PROMOTE FILTRATION
-The volume of tissue fluid increases dramatically and lymphatic drainage cannot always keep up = the excess tissue fluid stays in the tissue and edema occurs

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174
Q

BHP pressure change during inflammatory response

A

BHP = increased pressure
Cause of pressure change during inflammation: arteriole vasodilation increased blood flow into capillary bed

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175
Q

IFOP pressure change during inflammatory response

A

-Increased pressure
-Cause of pressure change during inflammation: Presence of microbial proteins, cell debris, and proinflammatory mediators in tissue fluid

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176
Q

BCOP pressure changes during inflammatory response

A

-Decreased pressure (only one that does down/decreases
-Cause of pressure change during inflammation: Normal: minimal effect
-If liver disease/dysfunction: hypoalbuminemia
-If kidney disease: Proteinuria

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177
Q

IFHP pressure change during inflammatory response

A

-Increased pressure
-Cause of pressure change during inflammation: arteriole vasodilation, increased venular vascular permeability, decreased lymphatic drainage

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178
Q

Filtration increased movement into ____

A

Tissues/interstitial fluid

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179
Q

Reabsorption increases fluid movement into ___

A

Blood stream/Blood plasma

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180
Q

Edema always causes an increase in this pressure

A

IFHP

181
Q

Mechanisms of Edema Formation

A

-Decreased synthesis of plasma proteins (cirrhosis, malnutrition) Increased loss of plasma proteins (nephrotic syndrome) Increased plasma sodium and H20 retention (dilution of plasma proteins) —> Decreased capillary Oncotic pressure —> Edema
-Increased capillary permeability (burns, inflammation) —> Loss of plasma proteins to interstitial space —> Increased tissue Oncotic pressure OR Decreased capillary onconic pressure —> edema
-Lymph obstruction —> Decreased transport of capillary filtration protein —> Increased tissue onconic pressure
-Increased Capillaru Hydrostatic pressure (venous obstruction, salt and water retention, heart failure) —> fluid movement into tissues —> edema

182
Q

Not all ___ is a result of inflammation

A

Edema

183
Q

More than 1 ___ can change in each situation

A

Pressure

184
Q

Clinical manifestations pressures Liver

A

Liver: Makes albumin, the major water regulator in blood plasma (regulates blood/capillary onconic P); decreased blood albumin causes decreased BCOP

185
Q

Clinical manifestations pressures Kidneys

A

Kidneys: any stressor will stimulate RAAS and increase aldosterone (regulates sodium and h20 retention by the kidneys); increased RAAS stimulation causes increased blood volume and increased BHP
Extreme imbalance may also decrease BCOP if plasma proteins diluted out

186
Q

Clinical Manifestations Pressures Burns

A

Burns: Cause damage to microvasculature + inflammation —> massive fluid shifts into the tissues
If blood proteins leak into the tissues, causes Increased IFOP

187
Q

Clinical Manifestations Pressure Infection

A

Infection: presence of microbial proteins + cell debris in interstitial fluid increase IFOP
This pressure will increase even more as inflammatory mediators enter the wound site

188
Q

Clinical Manifestations Pressure Lymphatic Drainage

A

Lymphatic Drainage: damaged local lymphatic vessels, infections and cancer cells can block lymphatic drainage through lymph nodes
When lymphatic drainage decreases, fluid accumulated in the tissues, causes increased IFHP

189
Q

Clinical Manifestations Pressure Hypertension

A

Hypertension: Leads to increased systemic BHP

190
Q

Clinical Manifestations Pressure Venous blood flow

A

Venous blood flow: obstruction leads to local increased venous BHP
Eg. Varicose veins

191
Q

Clinical Manifestations Pressure Heart Failure

A

Heart failure: leads to pulmonary (if left heart failure) or systemic (if right heart failure) increased venous BHP

192
Q

Edematous fluid is more specifically called

A

Transudate or exudate

193
Q

Main differences effected transudate vs exudate

A

Timing of production
Specific chemistry

194
Q

Why is excess tissue fluid important during inflammation?

A

-Purpose of inflammation is to dilute out injurious agents and bring in nourishment as well as WBCs to hopefully destroy foreign agents
-The fluid and debris within the damaged site will eventually make its way into the lymphatic capillaries and ultimately enter a lymph node or the spleen to be destroyed by various innate and if stimulated by the specific antigen, adaptive WBCs, thus also promoting wound healing

195
Q

Transudate

A

-Immediate, excess watery tissue fluid
-Essentially same chemical composition as normal tissue fluid produced during capillary exchange —> water, salts, electrolytes
-Result of Increased local blood flow and increased local blood hydrostatic P (due to arteriolar vasodilation)
-Most transudate is pushed out of dilated arterioles; capillaries have minor role
-Helps dilute out injurious agent

196
Q

Exudate: Fluid exudate

A

-excess tissue fluid rich in plasma proteins
-proteins help with innate and adaptive immune responses —> may contain antibodies, complement, clotting factors, cytokines to aid in pathogen destruction and wound healing

197
Q

Cellular exudate

A

-include the wbcs that infiltrate the injury site (in clotting, also includes platelets and rbcs)
-wbc phagocytosis of causative agent and cell debris aids in destroying pathogens and in wound healing

198
Q

Exudate

A

-Takes longer to begin, requires myoendothelial contraction to occur
-Most exudate flows out of venules since they have largest interendothelial cell gaps and greatest increased vascular permeability; capillaries have minor role
-Thicker consistency

199
Q

Normal Production of transudate and/or exudate: BHP

A

-Pressure of the blood plasma within a blood vessel, essentially water pressure
-Within the microvasculature, BHP is normally highest in arterioles and lowest in venules, so blood naturally flows in this direction
-BHP is a pushing pressure that pushes fluid out of the capillaries into the interstitium (tissue fluid) to nourish body cells

200
Q

Normal Production of transudate/exudate: BCOP

A

-Pressure of the plasma proteins to pull water towards them
-BCOP is a pulling pressure; pulling water towards the blood plasma chemical exerting osmotic pressure, albumin (most abundant plasma protein) and sodium

201
Q

Production of Transudate: Edema due to increased BHP varicose veins

A

-E.g due to obstruction of venous drainage (vericose veins) varicose veins damage venous valves and cause congestion of blood in the systemic veins. Local venous BHP increases and pushes fluid into the tissues leading to peripheral edema, especially common in the legs

202
Q

Production of transudate: Edema due to increased BHP Congestive heart failure

A

-CHF occurs when the heart muscle is too weak to pump blood effectively
-Also causes congestion of blood in either pulmonary or systemic veins
-Similar to obstructed venous outflow, that increased venous pressure causes back pressure to the microvasculature, increased venous BHP and pushes fluid into tissues

203
Q

Production on Transudate: Edema due to increased BHP Hypertension

A

-Dramatic increase in arterial BP causes increased BHP in the arterioles and capillaries
-Thus more fluid is pushed into tissues at the arteriole end of the capillary bed than can be reabsorbed at venule end of microvasculature

204
Q

Production of Transudate Edema due to decreased blood colloid osmotic/Oncotic pressure (BCOP)

A

-Eg liver or kidney disease
-Liver makes majority of your plasma proteins including albumin (albumin is a major regulator of water balance in blood plasma; exerts blood colloid pressure which means it pulls water towards it)
-Hypoalbuminemia causes a decrease in the osmotic pressure of albumin = Transudate fluid stays in the tissues causing peripheral Edema and leading to a decrease in blood volume
-Some kidney disorders result in a loss of plasma proteins into the urine, again leading to peripheral Edema

205
Q

Production of Exudate: What happens during acute inflammation

A

-During acute inflammation, due to rapid histamine mediated vascular response, local arteriole vasodilation causes increased local blood flow into the injury site
-This increases local capillary BHP
-Increased local BHP will push fluid from the blood into the tissues —> Transudate forms, then the endothelial cells contract, increasing venule and capillary vascular permeability allowing larger proteins to enter the interstitium
-= fluid exudate forms once the WBCs enter the wound site —> then cellular exudate forms

206
Q

Transudate Vs Exudate what makes them

A

Transudate if epithelial contraction DIDNT happen, pushing excess fluid into tissues, lymphatic system can’t keep up IFHP increases swelling
Exudate increase IFHP but also increased vascular permeability = cells/wbcs/proteins escape

207
Q

Cause of Edema: increased BHP

A

Composition of fluid in tissue space: Transudate
Local or systemic effects or both: Local and systemic Eg increased bp

208
Q

Cause of Edema: Deceased BCOP

A

Composition of fluid in tissue space: Transudate
Local or Systemic effects or both: Systemic (number of blood proteins decrease but not escape)

209
Q

Cause of Edema: Increased Vascular Permeability

A

Composition of Fluid In Tissue Space: Transudate or Exudate (Eg inflammation
Local or Systemic: Both

210
Q

Cause of Edema: Decreased lymphatic drainage

A

Composition of fluid in fluid space: Transudate or exudate depending on situation
Local or systemic: both

211
Q

Lewis’s Triple Response

A

-Illustrates the dermal microvasculature response to tissue injury that occur IMMEDIATELY (within 1-2 secs)
-Within several seconds: Histamine release by mast cells = The flush, The flare, The wheal

212
Q

Lewis Triple Response Vasospasm

A

-When a tissue is injured, 2 smooth muscle vascular effects occur in quick succession:
-Arteriolar vasospasm - immediate but brief as vascular smooth muscle contracts in response to sympathetic NS release of norepinephrine or epinephrine = transient vasoconstriction stress response to injury = white line
-Vasospastic response is quickly overwhelmed by the much larger mast cell degranulation and release of histamine
-= Arteriolar vasodilation - histamine mediated smooth muscle relaxation = vasodilation = redness + heat
-Venular increase vascular permeability -histamine mediated myoendothelial contraction = swelling

213
Q

The Flush

A

-Red line
-Due to onset of local arteriole (and passive) capillary vasodilation = occurs within seconds

214
Q

The Flare

A

-Bright red zone surrounding the red line
-Due to larger area of local arteriole vasodilation = Takes 15-20 seconds

215
Q

The Wheal

A

-Swelling at the site
-Due to fluid shift of intravascular fluid into tissues
-Caused by increased vascular permeability of local venules
-Takes 1-3 mins

216
Q

Why is triple response normally preceded by white line ?

A

Tissue injury hurts, it’s a stress response by SNS

217
Q

White line, Erythema, Edema Time frame, Cause, Mediator

A

White line; 1-2 seconds, SNS stimulated, quickly overwhelmed by mast cell degranulation and release of histamine
Erythema: 15-30 secs, Vasodilation of local arterioles, histamine
Edema: 1-3 seconds, increased vascular permeability, histamine

218
Q

Immune cells include

A

-all WBCs
-whether they reside in the tissues (mast cells and resident macrophages or dendritic cells) or in the blood stream (basophils, eosinophils, neutrophils, monocytes, b & t lymphocytes, NK cells)

219
Q

Mast cells and basophils

A

-secrete histamine and other Proinflammatory mediators

220
Q

Peripheral WBCs, platelets, RBCs, damaged endothelial cells or damaged parenchyma cells and any foreign invaders

A

-Can all release a variety of proinflammatory chemicals that act as chemotactic agents (distress signals), vasodilatiors, pain inducers or affect vascular permeability

221
Q

WBCs destroy pathogens using

A

Phagocytosis, making antibodies

222
Q

RBCs transport

A

Oxygen and carbon dioxide

223
Q

Platelets trigger blood

A

Coagulation/clots

224
Q

Innate Immune cells

A

Macrophages
Neutrophils
Dendritic cells
Mast cells
Basophils
Eosinophils
NK cells

225
Q

Adaptive immune cells

A

Lymphocytes, B/T

226
Q

Function Innate immune cells

A

First line of defence, identify , initiate specific adaptive immune response

227
Q

Functions adaptive immune cells

A

Destroy invading pathogens, make antibodies

228
Q

WBC’s that promote inflammation

A

-Mast cells
-Basophils
-Neutrophils

229
Q

WBCs that act as phagocytes

A

-Neutrophils
-Macrophages (monocytes derived)
-Dendritic cells
-B lymphocytes —> plasma cells
-NK cells
-Eosinophils (also secrete histaminase)

230
Q

WBCs that induce cell apoptosis my

A

-NK cells
-Eosinophils
-Cytotoxic T lymphocytes (cell mediated immunity)
-Aided by antigen presenting cells and helper t lymphocytes

231
Q

WBCs that boost innate and adaptive responses

A

-Helper T Cells (boost everybody)

232
Q

Surveillance cells of the Mononuclear Phagocyte System

A

-Includes innate WBCs that are located at common sites of entry of pathogens Eg. Epidermal/dermal and mucosal surfaces
-Eg. Dendritic cells within dermis/epidermis and mucous membranes
-Eg. Various fixed macrophages (usually M1 that reside in specific tissues) and wandering macrophages that tour the lymphatic system, blood stream and reside and function in specific tissue or organ

233
Q

Specific Macrophages That reside In Organs

A

-Kupffer cells in the liver
-Microglia in the brain
-Dust cells in the lungs

234
Q

How do WBCs recognize tissue damage?

A

-Innate immune cells have receptors that recognize and react to specific microbial membrane protein patterns or microbial by products or even chemicals released by own damaged body cells

235
Q

Apoptosis

A

-Programmed cell death
-Part of normal cell physiology
-Due to lack of use such as extra uterine smooth muscle cells after baby is born
-Or due to inflammatory response = targeted cell death due to the release of cytolytic enzymes by various WBCs

236
Q

APCs

A

-Antigen presenting cells
-Phagocytize, process, and present antigen fragments (pieces of antigen attached to a cell membrane protein called MHC) to cytotoxic T cells of the adaptive immune system
-If the cytotoxic T cell has a receptor that can bind to the antigen (TCR= T cell receptor) it will bind then attack the APC, release apoptotic enzymes thus destroying the antigen =cellular mediated immunity

237
Q

Development of Immune Function

A

-Born with some innate WBCs such as intravascular neutrophils and tissue mast cells but very few adaptive immune cells
-Adaptive immune function minimal at birth
-Begins to truly develop around 6 months, fully functional by 2 years of age
-By 1 year most children have fairly good immune response to infection

238
Q

More boosters =

A

More memory B cells = stronger/faster antibody response

239
Q

PMN

A

-Polymorphonuclear leukocytes
-I.e neutrophils

240
Q

The cellular response; Mast cells and Other immune cells

A

-While the mast cells are busy degranulation get and synthesizing Proinflammatory mediators to stimulate the inflammatory response in the tissues, other immune cells traveling in the blood stream need to enter the tissues to help

241
Q

Distress Signals

A

Other WBCs also respond to distress signals
Eg. Neutrophils, dendritic cells, and macrophages also have receptors that allow them to respond to chemicals released by injured, dead, or dying body cells and some microbial proteins

242
Q

Pus

A

-Made of a combination of dead and dying WBCs (mainly neutrophils), dead and dying body cells, and dead and dying bacteria

243
Q

WBC Response During Acute Inflammation

A

-WBCs respond to:
1) Increased Vascular Permeability
2) Injured Cell Distress Signals

244
Q

WBCs response to increased vascular permeability

A

-Increased vascular permeability causing slower local venule blood flow
-Slow blood flow allows WBCs to enter plasmatic zone —> adhere to endothelium —> WBC margination/pavement action —> diapedesis —> emigration —> cellular exudate produced

245
Q

WBC response to injured cell distress signals

A

-Cytokines and chemokines that promote WBC chemotaxis and infiltration into injury site

246
Q

Purposes of WBCs in wound site?

A

Phagocytosis or apoptosis of pathogens and cell debris —> destroy pathogens and promote healing

247
Q

During acute inflammation all 3 ___ cells will be affected by change in blood flow

A

-Blood cells
-As fluid leaks out of blood stream the local blood viscosity increases and local rate of blood flow slows down
-Rather than anti adhesion molecules, local endothelial cells start expressing cell adhesion molecules on their outer cell membranes
-Slower local blood flow allows time for blood cells to enter plasmatic zone, adhere to endothelium and then infiltrate damage site and help in the inflammatory response

248
Q

Phagocytosis

A

-Ingestion and enzymatic and/or peroxide digestion of cell debris, foreign material, microbes
-AIDS inflammatory response by removing causative agents and debris which promote would healing
-Function of most WBCs

249
Q

Apoptosis

A

-Programmed cell death via the use of cytolytic chemicals such as proteolytic granzymes and perforins
-Destroy the integrity of the targeted cells plasma membrane and the cell dies
-Used by innate NK cells and adaptive cytotoxic T cells and eosinophils

250
Q

WBC emigration into wound site is mediated by:

A

-Chemotaxis
-WBCs, especially neutrophils, respond immediately to a chemical trail of distress signals from damaged tissues

251
Q

Chemotaxis

A

-The directional movement of leukocytes in response to a chemical gradient (a chemoattractant)
-Common chemotactic agents: cell debris, microbes, proinflammatory chemokines and cytokines

252
Q

Margination (and Pavementation)

A

-Mechanism by which WBCs move to outer margins of vessels (into plasmatic zone), roll/tumble along the endothelium, adhere to endothelium
-Pavement the endothelium by binding to endothelial cell adhesion molecules, CAMS, made only during inflammatory response

253
Q

Diapedesis

A

-Mechanism by which WBC squeeze into wound site through the inter-endothelial gaps
-Gaps created when histamine stimulated myoendothelial contraction
-An amoeboid movement (flowing of cytoplasm against cell membrane, aided by cytoskeletal motility proteins, actin)

254
Q

Emigration

A

-The actual movement of WBCs from the intravascular to the extravascular space
-I.e wound site
-They follow the chemotactic trail right to the damage

255
Q

WBC emigration process takes

A

10 minutes

256
Q

Recognition and attachment of WBC to microbial chemicals of bacterium (CAMS)

A

-CAMS are cell adhesion molecules made by phagocytes in response to microbial chemicals or damaged cell products
-Help with WBC motility and with phagocytosis of the correct cell (I.e. those that should be eaten in the wound site)
-Some of these adhesion molecules are the cellular receptors WBCs use to recognize microbial or body cell chemicals: PRRs and PAMPs
-Other foreign proteins (antigens) and microbial proteins attached to antibodies as well as some complement proteins (C3b) also stimulate phagocytic cells to marginate, infiltrate the wound site, and then adhere to and ingest the cells/chemicals that need to be removed from the wound site

257
Q

% of neutrophils in blood

A

60-70

258
Q

Cytokines vs chemokines

A

Cytokines = communication between WBCs
Chemokines = alerts to something wrong

259
Q

What type of exudate is resultant of leukocyte infiltration/emigration into the wound site ?

A

Cellular exudate

260
Q

Adherence, Margination, and Diapedesis

A

1) WBC adherence to endothelial cells (notice endothelial cell contraction)
2) WBC margination and pavementation —> begin diapedesis
3) Diapedesis continues —> WBC emigration into wound site

261
Q

Chemotaxis, infiltration/emigration and phagocytosis

A

1) Chemotaxis - positive Chemotaxis as WBCs follow the chemotactic trail towards the wound site = help signal WBCs (ie they promote leukocyte infiltration)
2) Lots of WBCs (neutrophils here) have migrated/infiltrated the wound site
3) Phagocytosis occurs

262
Q

Leukocyte Emigration (aka leukocyte infiltration)

A

-Movement of WBCs from the blood into the damaged tissue site
-Controlled by chemotactic agents “distress signals” released by damaged cells, including damaged vascular endothelial cells, damaged parenchymal cells, and microbial chemicals
-Since the WBCs move toward the chemotactic agents, process is sometimes called positive Chemotaxis and the chemicals called Chemoattractants
-Running from the smell of a skunk is negative chemotaxis
-The WBCs are essentially blood hounds that follow the chemical scent to the damage site
-Neutrophils have the best nose to scent out distress chemicals and usually the first WBC to emigrate into the wound and arrive in large numbers
-Neutrophils have very short lifespans often only minutes and often become distress signals themselves
-lots of dead neutrophils in pus

263
Q

Apoptosis is used by

A

Innate NK cells, adaptive cytotoxic T cells, and eosinophils

264
Q

NK cells kill

A

Pathogenic cells and damaged body cells

265
Q

TC cells use

A

-Apoptosis to specifically kill “marked” cells = cells with unique foreign markers on their outer cell membrane
-Viral infected cells displaying foreign/viral Ag markers
-Antigen presenting cells (APCs) that have previously phagocytize and processed antigens into small fragments that are displayed on the outer cell membrane of phagocytic WBC
-TC cells bind to the antigen fragments, secrete cytolytic enzymes and destroy the entire APC
-Cancer cells with unique foreign antigen/tumour markers

266
Q

Eosinophils kill

A

-Parasites by apoptosis
-Also phagocytize and destroy antigen-antibody complexes

267
Q

Unsuccessful Phagocytosis: Tonsils

A

-In some people, macrophages living in tonsils become breeding grounds for bacteria such as pustule forming streptococcus
-Tonsils will need to be removed
-Happens when phagocytosis is not successful =chronic infection

268
Q

Platelet response occurs if

A

Blood vessel wall is damaged during injury, are they bleeding

269
Q

Platelets respond to

A

1) Loss of endothelial cells due to blood vessel wall damage —> allows platelet-collagen interaction —> platelet activation occurs
2) Slower/more viscous blood flow —> resulting from increased vascular permeability during inflammatory response —> allow platelets to adhere to damaged blood vessel wall

270
Q

Platelet activation includes

A

Platelet adherence —> platelet release reaction —> platelet plug formation —> Hemostasis

271
Q

Purpose of platelet activation

A

Initiate hemostasis and blood coagulation to prevent further blood loss

272
Q

Platelets respond to tissue damage by

A

Initiating hemostasis and if necessary blood clotting

273
Q

Hemostasis

A

Defined as the stoppage of blood flow (to prevent excessive bleeding)

274
Q

Blood Coagulation

A

Formation of thrombus (if intravascular clot) or blood clot (if extravascular clot)

275
Q

Components of blood clot

A

Platelets, sticky fibrin threads and trapped RBCs

276
Q

Inflammation and platelet activation collagen

A

-Endothelial damage and resultant inflammation can trigger platelet activation
-In an inflamed blood vessel there is a lack of endothelial anti adhesion proteins and increased vascular permeability
-Platelets can enter the plasmatic zone and adhere to the endothelium
-Where endothelial cells are damaged, platelets may interact with collagen
-Since collagen is a connective tissue component located directly outside of the endothelium, platelet-collagen interaction in a damaged vessel is expected

277
Q

Inflammation and platelet activation slowed blood

A

-During inflammation, increased vascular permeability, especially at the venule end of the capillary causes a slight decrease in the blood pressure in the venule
-This slows the rate of blood flow allowing platelets time to enter the plasmatic zone
-Increases the chance of platelet-collagen interaction and platelet activation
-Activated platelets become sticky, try to plug the wound in the vessel wall and stimulate blood clot formation
-Since tissue damage often includes damage to blood vessels and bleeding, blood clot formation is an important part of the acute inflammatory response

278
Q

All blood vessels are lined with ..

A

-Endothelial cells (tunica intima)
-Regardless of the size of the blood vessel, directly beneath the intimal endothelium there will always be connective tissue
-Means there will always be the protein collagen

279
Q

What NSAID blocks thromboxane A2

A

ASA = anticoagulant because it blocks thromboxane synthesis

280
Q

Platelet Plug Formation: 1 Platelet adhesion

A

1) Platelet adhesion - Damage to endothelial lining —> platelet contact collagen —> platelets adhere to vessel wall endothelium

281
Q

Platelet Plug Formation: 2 Platelet Release Reaction

A

-Platelets secrete prothrombotic chemicals that make them enlarge and become “sticky” including PDGF, serotonin, thromboxane A2, ADP
-ASA would block thromboxane

282
Q

Platelet Plug Formation: 3 Platelet Aggregation

A

-Platelets may successfully plug the wound and stop the bleeding by forming a platelet plug
-If still bleeding now you need coagulation (clotting) cascade

283
Q

Thrombocytopenia/Thrombocytosis

A

Thrombocytopenia = patients bleed longer
Thrombocytosis = probe to dangerous intravascular thrombotic events

284
Q

RBC’s Respond to … during acute inflammation

A

1) Slower local blood flow —> resulting from increased venule vascular permeability during inflammatory response and/or
2) Platelet activation

285
Q

RBC activation includes:

A

RBC adherence —> Rouleaux formation —> followed by extravasation (RBCs move into extravascular spaces)… bleeding into tissues —> RBCs help form extravascular blood clot

286
Q

Purpose of RBC response

A

Help limit blood loss by strengthening and stabilizing blood clot

287
Q

RBC Response During Acute Inflammation

A

-During acute inflammatory response, increased vascular permeability increases tissue fluid causing blood remaining in local vascularture to thicken a bit
-This slower, thicker blood flow allows RBCs to enter plasmatic zone, RBCs may begin to stack up and then spill out of the vessel where they become trapped in a blood clot that was triggered by the platelets

288
Q

Rouleaux

A

The stacking up process

289
Q

Extravasation

A

-Process of blood cells leaving a blood vessel
-Extravasated RBCs will be trapped by the proteinaceous clotting fibers called fibrin threads and become part of the blood clot
-Form bruises and hematomas
-During wound healing they will need to be removed with some proteinaceous enzymes (Eg plasmin) and the help of hungry macrophages

290
Q

Initial transient arteriolar vasoconstriction due to autonomic sympathetic NS release of

A

Epinephrine/Norepinephrine

291
Q

Plasma protein systems

A

-complement system
-clotting system
-kinin system
-these are cascades of pro-inflammatory proteins that because activated during tissue damage
-pre formed proteins (made in advance) are circulating in the blood plasma as soluble inactive proteins

292
Q

What happens if plasma proteins fail

A

-if one or more proteins in insufficient or fails to activate, cascade fails leading to a lesser effect of that acute phase protein system in inflammatory response
-will delay or even prevent a proper acute inflammatory response allowing causative agent to survive and cause further damage/blood loss

293
Q

Defective protein synthesis is the result of —- or —- Etiology

A

Congenital, Genetic

294
Q

Lack of clotting protein is a cause of

A

Hemophilia

295
Q

What are the plasma protein systems?

A

-3 interrelated groups of Proinflammatory plasma proteins —> activated by tissue damage —> cascade effect
-Part of fluid and cellular exudate
-Part of inflammatory soup/cytokine storm
-Part of acute phase proteins

296
Q

Fluid exudate includes

A

Transudate plus proteins = fluid exudate includes the proteins of the 3 plasma protein systems (still present in cellular exudate)

297
Q

Since plasma proteins are activated during acute inflammatory responses they are also called

A

Acute phase proteins or acute phase reactants

298
Q

Other acute phase proteins include:

A

Chemokines and cytokines and systemic inflammatory marker called C-reactive protein (CRP)

299
Q

All proteins are produced when specific

A

Genes are turned on (expressed) and protein synthesis occurs
-over expression of a gene could cause overproduction of a particular protein which could cause exaggeration of that particular plasma protein pathway

300
Q

General Characteristics Plasma Protein Systems

A

-Produced by liver and/or WBCs
-Most produced in advance; circulate in blood plasma as inactive proenzymes
-Peak activity 10-40 hours post tissue damage

301
Q

How do plasma proteins work (mechanism of activation)

A

When tissue damage occurs —> inactive circulating proenzymes —> convert to active enzymes —> cascade of enzyme activation —> promote inflammatory response

302
Q

How plasma proteins act as Proinflammatory mediators

A

-Support and maintain the histamine response
-Help prevent further blood loss
-Part of acute phase proteins/reactants

303
Q

If you need more plasma proteins..

A

1) WBC’s release cytokines (interleukins IL-1 or IL-2) —> stimulate liver to produce more and or/
2) Produced in situ by damaged body cells (ie chemokines)
3) If systemic issue C reactive protein

304
Q

Inactive protein proenzyme prevents

A

Unnecessary, potentially harmful enzymatic activation within healthy tissues such as the liver cells or WBCs in which they are produced

305
Q

In response to tissue damage inactive proenzymes …

A

-enter the injured tissues, become activated enzymes (the enzymes are proteases that change the protein structure of the next inactive enzyme in the pathway and catalyze/speed up different proinflammatory chemical reactions such as signalling more WBCs, promoting blood clotting or maintaining vascular responses)
-Tissue damage will initiate the enzymatic activity of one or more components of a particular system
-Once the first protein in a particular plasma protein system is activated, domino effect occurs resulting in activation of remaining proteins of that system

306
Q

Plasma proteins have_____ functions

A

Overlapping
Safety net to ensure that inflammatory response is successful

307
Q

Complement proteins stimulated by

A

Inflammatory response to bacterial and yeast infections and by Ag-Ab reactions

308
Q

Clotting proteins stimulated by

A

Damage to vascular wall ie bleeding

309
Q

Kinin proteins are stimulated by

A

Microvascular response to tissue damage, acts like a weak histamine

310
Q

Inflammatory mediators (aka inflammatory markers) can be measured in

A

Blood plasma
Their specific levels and types help determine severity of inflammation

311
Q

Increase complement proteins =

A

Bacterial, yeast infection, or Ag-Ab response; local or systemic inflammatory response

312
Q

Increase clotting proteins =

A

Microvascular damage, local or systemic inflammatory response

313
Q

Increase CRP

A

Systemic inflammatory response

314
Q

The complement system

A

-Innate immune response (2nd line of defence)
-Series of 9 plasma proteins (C1-C9)
-Source: liver

315
Q

Complement system mechanism of activation

A

-3 pathways of complement protein activation (require some type of causative agent)
1) Classical pathway - antibody present
2) Lectin pathway - bacterial polysaccharide (mannose) present
3) Alternative pathway - bacteria lipopolysacharides or yeast carbohydrates present

316
Q

If inactive/active

A

Inactive = proenzyme: C1, C3
Active = functional enzyme: C1a, C3a, C3b

317
Q

C1-C9 means

A

Complement protein is inactive

318
Q

C1a-C9a means

A

This protein is now active and triggering activation of the next complement protein in the pathway

319
Q

If proenzyme is cleaved into 2 parts

A

Both are active

320
Q

Physiological effects of complement protein activation

A

-Form membrane attack complexes (MAC); C5b-C9 destroy cell membrane of causative agent
-Act as opsonins (opsonization); C3b to make tasty
-Act as leukocyte chemotactic agents; attract phagocytes to site (WBC infiltration) = promote phagocytosis; C5a
-Act as anaphylatoxins - stimulate mast cell degranulation —> histamine release; C3a or C5a; part of anaphylaxis
-Attract antibodies to wound site; C1a

321
Q

End result of complement activation

A

Promote inflammation and help destroy pathogens

322
Q

Membrane Attack Complex (MAC)

A

-C5b-C9
-Complement protein complex pokes holes in the outer cell membrane of the bacterium leading to cytolysis
-E.g makes bacterial walls leaky to water —> bacteria lysed/contents leak out —> bacterium dies

323
Q

Opsonization

A

-C3b
-This complement protein will sugar coat the surface of the antigen to be phagocytized helping to attract phagocytes and make the process of phagocytosis more efficient

324
Q

Chemotactic agents and anaphylatoxins

A

-C3a and C5a
-Promote WBC infiltration
-Especially attract phagocytic neutrophils, macrophages and dendritic cells to damage site and stimulate rapid mast cell degranulation = histamine release
-Histamine then stimulates inflammatory response

325
Q

The coagulation (blood clotting) system

A

-A group of 12 plasma proteins (factors I-XIII; active Xa
-aka clotting factors
-Sources; liver (major) and as required by platelets or other damaged cells

326
Q

Coagulation system mechanism of activation

A

1) -Endothelial damage occurs —> platelet-collagen interaction in damaged blood vessel —> platelet activation
2) Blood flow stasis —> platelet activation
-platelet activation leads to sequential activation of clotting factors of the coagulation cascade —> sticky fibrin threads form
-RBCs and platelets trapped in sticky fibrinous mesh —> blood clot forms

327
Q

End result of clotting factor activation

A

Hemostasis to stop the bleeding

328
Q

The clotting system is part of the process called

A

Hemostasis

329
Q

Why is Hemostasis including the clotting system involved during acute inflammation

A

-Tissue injury often involves damage to the blood vessels in the area (bruise, cut)
-When a blood vessel is damaged, RBCs spill out of the vessel = extravasation
-Platelets become activated, as the process of Hemostasis occurs to try to prevent excessive blood loss

330
Q

2 Routes to Activation of the Clotting Cascade

A

1) Extrinsic Pathway
2) Intrinsic Pathway

331
Q

Extrinsic Pathway Clotting Cascade

A

-More common pathway, cuts/bruises
-Tissue damage stimulate/activates
-released by damaged parenchymal and stromal cells = release tissue factor (TF, Factor III)
-TF (IIIa) —> Factor X activated (Xa)—> Common pathway of Coagulation triggered

332
Q

Intrinsic Route clotting Cascade

A

-Activated by factors in blood; Endothelial cells damage (Eg. Arteriosclerosis, phlebitis, arteritis)—> platelet-collagen interaction —>Platelet activation —> Factor XII activated (Xa) —> coagulation cascade
-XII—>XIIa—>Xa—> Common Pathway of Coagulation

333
Q

Common Pathway of Coagulation

A

Xa—> Prothrombin (II) —> Thrombin (IIa)
Fibrinogen (I) —> Sticky Fibrin (Ia) Threads —> Blood Clot (Coagulation)

334
Q

FP =

A

-Fibrinopeptides
-Cleaved (I.e. cut) from fibrinogen
-Chemotactic for neutrophils and increase vascular permeability (by increasing kinin effects)

335
Q

Both intrinsic and extrinsic pathways meet at the

A

Common pathway of coagulation initiated by Factor X (Xa) and ending with the conversion of the inactive soluble protein Fibrinogen (proenzyme) to active insoluble Fibrin threats

336
Q

Fibrin threads form…

A

Sticky mesh work of a blood clot

337
Q

___ and ____ stick to the mesh work

A

Platelets and RBCs
Create a larger plug to hopefully stop the bleeding

338
Q

Endothelial damage allows ___ and ____ to interact

A

Platelets and CT collagen

339
Q

Clot should remain until

A

-Wound healing is well underway

340
Q

Clot Dissolution

A

-The enzymatic (via plasmin) digestion of fibrin + macrophage phagocytic destruction of old trapped RBCs and platelets that occurs during wound healing

341
Q

Factor XII

A

-Hageman Factor
-XII denotes (indicates) inactive clotting factor
-XIIa denotes the active clotting factor

342
Q

Cofactors required for blood clotting include

A

-Ca
-K

343
Q

The coagulation cascade is a ____ feedback system

A

-Positive
-since clotting mechanisms continue either until the bleeding has stopped or supply of clotting proteins is exhausted

344
Q

Blood clotting disorders are a result of

A

-an inability to produce one or more biologically active clotting factor
-common inherited form of hemophilia is due to genetic defect in production of factor VIII
-Dietary or nutrient absorption issues with calcium or decrease liver production of Vit K can also impede

345
Q

Clotting factor 1

A

Fibrinogen
-Source: Liver
Pathway of activation: Common

346
Q

Clotting Factor 2

A

Prothrombin
-Source: Liver
-Pathways: Common

347
Q

Clotting Factor 3

A

Tissue Factor (Thromboplastin)
-Source: Damaged Tissues and Activated Platelets
Pathways: Extrinsic

348
Q

Clotting Factor 10

A

Stuart Factor, Prower Factor, Thrombokinase
-Source: Liver
-Pathway: Extrinsic and Intrinsic

349
Q

Clotting Factor 12

A

Hageman Factor, Glass Factor, Contract Factor or Antihemophilic Factor C
-Source: Liver
-Pathway: Intrinsic

350
Q

Clotting Factor 4

A

Calcium
-Source: Diet, Bones, Platelets
-Pathway: All

351
Q

Fibrinogen is the

A

Last inactive factor to be activated but more obvious clotting pathway

352
Q

If ends in Ogen/Pro =

A

Inactive form

353
Q

Factor _ must be activated to start clotting

A

10

354
Q

Extrinsic = Intrinsic =

A

Bruising, cuts / DVT

355
Q

If trigger XIIa

A

Activates kinin system

356
Q

Components of a blood clot or thrombus

A

-RBCs
-Platelets
-Fibrin threads

357
Q

Thrombus

A

Denotes intravascular blood coagulation (intrinsic pathway)

358
Q

Blood clot

A

Denotes extravascular blood coagulation Eg bruise, hematoma, contusion (extrinsic + intrinsic pathway)

359
Q

Trigger that starts the cascade

A

Slowed blood, interaction with collagen

360
Q

Functions of a Blood Clot

A

1) Plug damaged vessels to stop further bleeding
2) Trap microbes to prevent spread of infection
3) Provide a framework for wound healing

361
Q

Fibrous Network =

A

A mesh like collection of sticky fibrin threads

362
Q

Colours of a bruise/hematoma

A

Correspond to the breakdown of the hemoglobin in the extravasated RBCs as they are phagocytized by Macrophages

363
Q

Colours of bruises

A

Red (acute inflammation) —> black —> blue —> green —> yellow

364
Q

Clot dissolution

A

Once wound healing is complete and damaged blood vessel have new intact endothelial PLASMIN will dissolve the blood clot by breaking up fibrin threads
-local MACROPHAGES Will chew up the clot components that were trapped within tissue cells

365
Q

The Kinin System

A

-Group of 4 Plasma Proteins
-Source: Liver (major) and many other body cells
-Mechanism of Activation; Tissue damage (Prekallikrein is activated by Factor XIIa of clotting cascade —> bradykinin)

366
Q

Kinin helps maintain…

A

The inflammatory response

367
Q

Physiological effects of kinins

A

-Bradykinin has similar but less potent effects than histamine
-Arteriole vasodilation—> redness, heat
- Increased vascular permeability—> Edema
-Acts as Chemotactic agent for WBCs
-Pain stimulant (works with prostaglandins to irritate nerve endings)

368
Q

Factor __ activated prekallikrein

A

Factor XII aka Hageman factor
-activated prekallinkrein in Kinin pathway = creation of bradykinin

369
Q

Bradykinin stimulates

A

Vascular smooth muscle relaxation and myoendothelial cell contraction

370
Q

Kinin cascade and ___ have interrelated functions

A

-clotting cascade
-chances are if inflammatory response is occurring, blood vessel is also damaged and bleeding is present

371
Q

Kinin cascade activated by

A

-XIIa Factor of clotting system
XIIa —> prekallikrein —> Kallikrein —> Kininogen —> Bradykinin —> histamine effects and pain

372
Q

Activation of Kinin pathway can trigger

A

XIIa and Factor XIIa can trigger Kinin pathway

373
Q

Secretions that contain Kinin

A

Tears, sweat, saliva, urine, feces
Help mediate local inflammatory response

374
Q

Inflammatory regulators/anti-inflammatories

A

Carboxypeptidase, Kinase, Plasmin, Histtaminase

375
Q

Why are inflammatory regulators/anti inflammatory chemicals needed

A

Once problem has been resolved and the tissue begins to heal, anti-inflammatory signals must be present to turn off secretions of pro-inflammatory histamine, complement, clotting and Kinin proteins and to release any trapped RBCs and platelets by dissolving fibrin threads

376
Q

Inflammatory regulators made by

A

Usually enzymes
Made by the liver, endothelial cells, immune cells and/or healing body cells

377
Q

Inflammatory regulators also know as

A

Proteolytic enzymes

378
Q

Carboxypeptidase

A

Effects C3, Inactivates anaphylatoxic C3a and C5a (leukocyte/neutrophil migration)

379
Q

Kinase

A

Inactivates Kinin pathway

380
Q

Plasmin

A

Lots of anti inflammatory effects
Activated form of inactive plasma protein plasminogen made by endothelial cells, monocytes, macrophages

381
Q

Plasmin activity

A

Anticoagulant - decreases activation of factor XIIa and thrombin thus effects both intrinsic and common pathways of coagulation, limits size of clot, and involved in clot dissolution (aka fibrinolysis = destruction of blood clots) destroys fibrin threads that trap platelets and RBCs
Decreases complement activity (turns of C3, occurs once Ag-Ab complexes in damaged tissues have been cleared by eosinophils; decreases rate of WBC infiltrations and phagocytic activity, helps decrease histamine levels

382
Q

Histaminase

A

Made by eosinophils that enter wound site, Inactivates histamine remaining In tissue fluid at end of inflammatory response

383
Q

Effects of over production of complement proteins

A

Excessive inflammation and histamine secretion —> hypersensitivity reaction

384
Q

Effects of Overproduction of clotting proteins

A

Hypercoagulability

385
Q

Effects of overproduction of Kinin proteins?

A

Excessive inflammation —> hypersensitivity reaction and pain

386
Q

Inflammatory soup contains

A

ALL chemical mediators found in fluid and/or cellular exudate that promote inflammation including plasma derived mediators and cell derived mediators

387
Q

Inflammatory soup is

A

Fluids only no solids = Fluid exudate (proteins)

388
Q

What’s in inflammatory soup

A

1) Plasma Derived Mediators
-Includes 3 plasma protein systems (complement, clotting, kinin and CRP)
2) Cellular Derived Mediators
-Local parade one or autocrine effects
-Made by a variety of WBC’s, platelets, endothelial cells and/or injured cells activated by tissue damage
-Includes cytokines and chemokines
-chemicals made by cells but NOT cells themselves
-All Proinflammatory mediators may become part of soup during inflammatory response, they are part of fluid/cellular exudate

389
Q

Cytokine Storm

A

When damaged tissues and the immune system create too many cytokines and chemokines, inflammation can overwhelm the tissues causing extensive tissue damage
Eg. Covid 19 and lung damage

390
Q

Inflammatory soup =

A

Cytokine storm
-Issue with cytokine storm name is that it does not include other proinflammatory chemicals (chemokines, acute phase proteins, even histamine) but they are also present and causing excessive inflammatory damage

391
Q

How are cytokine storms treated

A

Antihistamines

392
Q

Prolonged inflammatory response =

A

Systemic effects such as
Fever
Leukocytosis (increased production of leukocytes)
Increased plasma levels of specific cytokines and CRP

393
Q

Vascular, cellular and protein responses to tissue damage present in both ___ and ___ clinical manifestations

A

Local, and/or systemic

394
Q

Local Manifestations of Acute Inflammation

A

-Extent will depend on severity of tissue damage
-5 Cardinal signs of inflammation will be present to some degree
Type of local inflammatory fluid : presence of transudate, fluid exudate, or cellular exudate depends on location and cause of damage

395
Q

Types of Local Inflammatory Exudate

A

1) Serous Exudate
2) Fibrinous Exudate
3) Purulent/Suppurative Exudate
4)Hemorrhagic Exudate

396
Q

Serous Exudate

A

Thin, Clear, Straw-coloured, watery fluid, similar to Transudate (minimal proteins)
Small amount normal during inflammation (Eg blister), copious amounts not normal = infection possibly

397
Q

Fibrinous Exudate

A

Contains lots of proteins such as fibrin and fibrinogen, thick/viscous, usually lots of fibrin

398
Q

Fibrinous vs fibrous

A

Do not confuse
Fibrous tissue contains excess collagen Eg a scar

399
Q

Purulent/Suppurative Exudate

A

Contains pus, abscesses or cysts may be present, infected

399
Q

Purulent/Suppurative Exudate

A

Contains pus, abscesses or cysts may be present, infected

400
Q

Hemorrhagic exudate

A

Significant bleeding occurred, contains thick gel like coagulated blood (blood clots)

401
Q

Hemorrhagic exudate

A

Significant bleeding occurred, contains thick gel like coagulated blood (blood clots)

402
Q

Serous fluid found in

A

A) characterized by copious effusion (excess tissue fluid accumulation) of watery fluid with very little protein
-found in early inflammatory response or in mild injury such as a blister
-if clear and pink may be called serosanguinous exudate
B) Pleurisy = inflammation of pleural membranes = causing serous fluid buildup in pleural cavity = atelectasis = lung collapse

403
Q

Fibrinous Exudate means

A

Large amount of protein is present in exudate
Occurs with more severe injury resulting in large increase in vascular permeability which allows plasma proteins to pass through large interendothelial cell gaps in blood vessels and deposit in tissues
Since fibrin is protein that creates clotting fibers, excess fibers create coagulated exudate that covers surface of area such as body cavity (pericarditis, pleurisy, pneumonia, peritonitis)

404
Q

Clinical significance Fibrinous Exudate

A

Body cavities and internal organs are surrounded by serous membrane that secrets thin watery lubricating serous fluid, Fibrinous Exudate impairs normal ability of organs in cavaities to move freely as the function = in pericarditis heart can’t pump properly

405
Q

What are pustules?

A

Pus filled blisters/ lesions

406
Q

Pus forming bacteria are called

A

Pyogenic
Eg. Staphylococchus

407
Q

Pus may become ..

A

Walled off in a cyst or abscess = must be evacuated in order for wound healing to occur

408
Q

Term for removal of Purulent exudate

A

Evacuation

409
Q

Hemorrhagic exudate means

A

Blood vessels have ruptured, bleeding has occurred and a blood clot is present
Contains extravasated blood cells, clotting factors (platelets, RBCs, fibrin)

410
Q

Effects of inflammation on lymphatic system local

A

If tissue is bleeding, small lymphatic vessels have also been damaged
Part of time it takes swelling to go down is time it takes to heal lymphatic capillaries so they can start draining excess tissue fluid and lymph away from tissues

411
Q

Effects of inflammation on lymphatic system systemic

A

Because lymph capillaries are more permeable than blood capillaries, they often are conduits for spread of infection or neoplastic cells = reason that regional lymph node biopsy is completed for suspected cancer

412
Q

Key points of inflammation on lymphatic system

A

Locally, lymphatic vessels and organs can also be damaged by direct mechanical trauma (acquired Etiology)

413
Q

Lymphatic capillaries are ___ so they can pick up excess ___

A

Leaky, tissue fluid
-makes them excellent conduits of transport

414
Q

Lymphatic capillaries may become inflamed due to

A

1) local or systemic spread of infections
2) blockage by neoplastic cells (metastasis)

415
Q

Lymphedema

A

Excessive swelling of tissue due to blockage or loss of lymphatic flow (decreased lymphatic drainage)
-caused by last slide

416
Q

Clinical manifestations of lymphatic tissue inflammation

A

Lymphadenopathy
Lymphadenitis
Lymphangitis

417
Q

Lymphadenopathy

A

-Enlarged lymph node or nodes
-palpable swelling of 1 or more lymph nodes with little or no tenderness/pain
-Eg. Upper resp infection with enlarged cervical lymph nodes
-Eg. Lymphoma or Cancer metastatic lymph node involvement

418
Q

Lymphadenitis

A

Painful, inflamed lymphadenopathy (enlarged lymph nodes)
Usually due to infection
Shows signs of inflammation (redness, tenderness)
-Eg. Tonsillitis
-E.g infectious mononucleosis (Epstein-Barr virus)

419
Q

Lymphangitis

A

Inflammation of lymphatic vessel due to infectious or non infectious causes
Follows direction of lymph drainage (towards heart)
Watch for red streaks radiating towards heart
High risk of systemic infection

420
Q

Systemic manifestations of acute infection indicate

A

Tissue damage/infection is spreading to other body regions

421
Q

Major systemic manifestations acute inflammation

A

1) fever (pyrexia) -pyrogens present
2) leukocytosis - increased WBC count
3) increase acute phase reactant proteins in blood plasma
4) increase in CRP in blood plasma
5) may also include: malaise, drowsiness, poor appetite, increase liver production of fibrinogen, decrease liver production of albumin, hypotension

422
Q

Fever stimulated by

A

Stimulated by pyrogens tricking thermoregulatory centres of hypothalamus

423
Q

Leukocytosis

A

Increased number of WBCs
-during systemic acute inflammatory response to infection 2-3 fold increase of WBC count may occur (some WBC such as eosinophils are rare

424
Q

Differential WBC count

A

-Used to detect change in number of rare WBCs such as eosinophils
-Determines % of each subtype of plasma WBC within total plasma WBC population
- increased neutrophils = acute inflammation
-Increased monocytes = chronic inflammation
-Increased lymphocytes = viral infection
-Increased eosinophils = parasitic infection or large number of Ag-Ab complexes present

425
Q

Acute Phase Reactant Proteins and systemic acute inflammation

A

Fine oven levels increase if bleeding is occurring
Albumin production decreased as liver spends it resources on acute inflammatory protein production
Since albumin major regulator of intravascular fluid volume (BCOP) during capillary exchange, blood volume decreased as fluid enters tissues = loss of blood volume = hypotension

426
Q

What is used to diagnose inflammatory disease

A

Body T
Differential WBC count
Inflammatory protein plasma markers

427
Q

Fever (pyrexia)

A

Elevation of core body temp above hypothalamic set point of 37C

428
Q

Pyrogens

A

-Fever inducing chemicals that can change hypothalamic T set point
-2 Types Endogenous pyrogens, Exogenous pyrogens

429
Q

Purpose of fever?

A

To inhibit bacterial growth

430
Q

Complications of fever

A

-tissue damage to cellular proteins (denaturation)
-Increase bacterial endotoxin associated tissue damage
-Increased demand for 02 and glucose
-Dehydration, lethargy, malaise, hypotension, rapid HR

431
Q

Body T is controlled in the

A

Hypothalamus of the brain
Specifically in the hypothalamic thermoregulatory Center
-senses changes in temp of blood and CSF flowing in the hypothalamus

432
Q

Endogenous Pyrogens

A

-Cell derived cytokines (IL-1, TNF) made by neutrophils and macrophages after exposure to tissue damage or antigen-antibody complexes
-Elliot a fever response

433
Q

Exogenous Pyrogens

A

-Bacterial lipopolysaccarhides (LPS), bacterial exotoxins, bacterial endotoxins that are released as bacteria are destroyed, viral proteins, ag-Ab complexes, some drugs

434
Q

Course of Fever

A

1) release of pyrogens (exo or endo)
2) pyrogens trick hypothalamus into thinking core body temp is too LOW = hypothalamus responds by stimulating shivering to 3) INCREASE body temp thus 4) higher body temp that manifests as fever 5) treatment of pyrogens means that either WBCs are busy phagocytize for those pyrogens microbes or you take fever reducing drug = decreased pyrogens in your blood 6) hypothalamus notices you are too hot and 7) starts physiological mechanism of sweating that reset thermostat back to normal

435
Q

If INCREASE in pyrogens in your blood/CSF

A

Hypothalamus thinks your cold = you shiver and your body heats up

436
Q

If decrease pyrogens in blood/csf

A

Hypothalamus thinks ur too hot, you sweat and body cools down

437
Q

Fever also increases

A

Oxygen consumption by hot tissues = increased HR
Could be detrimental in a cardiac patient whose body cannot tolerate increased work load

438
Q

Leukocytosis systemic

A

-Diagnosed by differential WBC count
-Acute inflammation:
Increase number of circulating phagocytes (neutrophils, monocytes)
Increase number of tissues phagocytes (macrophages and dendritic cells
Increase number of specific WBC determined by infective agent

439
Q

Increased acute phase plasma proteins systemic acute inflammation

A
440
Q

Possible outcomes of acute inflammation

A

Chronic inflammation occurs when the combined efforts of the vascular, cellular and plasma protein responses have not successfully cleared the causative agent

441
Q

Major immune cell types chronic inflammation

A

Lymphocytes (long enough to trigger adaptive immune response) and macrophages
Fibroblasts also present since chronic inflammatory sites are prone to excessive scar tissue formation

442
Q

Chronic inflammation is stand-off between

A

Host defences and causative agent

443
Q

Chronic inflammation essentially

A

An unsuccessful acute inflammatory response

444
Q

Etiology Chronic Inflammatory Response

A

Continuous presence of causative agent:
-Infection: Chronic tonsillitis, tuberculosis, HIV, Hep C
-Foreign body: shrapnel, asbestosis
-Foreign Antigen: tissue/organ transplant rejection, allergy (hypersensitivity) reactions
-Self antigen: autoimmune reactions
Repetitive injury
-Osteoarthritis, repetitive strain injuries, carpal tunnel syndrome, workplace chemical exposure

445
Q

Chronic Inflammatory response and scarring problem

A

Weaker than normal tissue, prone to reinjury

446
Q

Chronic inflammation or chronic inflammatory response develops when

A

Vascular (Lewis’s triple) response, innate and adaptive immune cellular response, plasma protein activations could not destroy and remove cause of tissue damage

447
Q

Within Chronic inflammatory site…

A

There will be areas of new acute inflammation and areas of various stages of wound healing

448
Q

Things that increase chance of chronic. Inflammation

A

Age (very young/old), immunocompromised, hypersensitivity immune reaction to repeat exposure, virulence of infectious agent, strength and duration of toxic exposure, repetitive reinjury

Pathophysiology (8 decks)

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