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pathophysiology 1 > Module 2: Inflammation > Flashcards

Module 2: Inflammation Flashcards

1
Q

What are the two types of immune defenses?

A

1) innate– fast but non-specific and is both the 1st and 2nd line of defense

2) adaptive– slow but very specific and is the 3rd line of defense

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2
Q

Describe the innate immune response

A

fast, non-specific to particular antigens, ex. mucous production

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3
Q

Describe the adaptive immune response

A

very specific response to a very specific antigen– this response is developing between 6 months and 2 years of age

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4
Q

What causes acute inflammation?

A

any breach of body defenses results in an immediate, localized response to damage (acute inflammation)

if the issue is not resolved then it may result in chronic inflammation

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5
Q

What is the difference between first line of defense and second line of defense?

A

first line– physical barriers, biochemical barriers, and normal microbiome

second line– antimicrobial substances (ex. cytokines), and immune cellular defenses (innate WBC functions such as apoptosis), inflammatory response, and fever

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6
Q

Describe the third line of defense (adaptive immunity)

A

2 lymphocyte types with difference mechanisms of destroying the antigen

1) humoral (antibody mediated) immunity (B lymphocytes)
2) cell mediated immunity (T lymphocytes)

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7
Q

What is humoral immunity?

A

also called antibody mediated immunity, part of the third line of defense

B lymphocytes–> differentiate into plasma cells–> production of specific antibody/immunoglobulin which binds to and results in destruction of antigen

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8
Q

What is cell mediated immunity

A

part of the third line of defense

T lymphocytes–> production of antigen specific helper T cells (stimulate other T and B cells) and cytotoxic T cells–> bind to and stimulate apoptotic destruction of antigen containing cell

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9
Q

What are the two key features of adaptive immunity?

A

1) specificity– each B or T cell responds to one specific type of antigen

2) immunological memory– each B or T cell remembers the antigen and subsequent re-exposure elicits a rapid response (so fast that no symptoms of illness should appear)

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10
Q

What is included in the microscopic blood vessels?

A

arterioles, capillaries, and venules

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11
Q

Describe the arterioles

A

they vasoconstrict and vasodilate to control local capillary bed blood flow to tissues

contain smooth muscle

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12
Q

Describe the capillaries

A

sit of nutrient and gas exchange

do NOT contain smooth muscle

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13
Q

Describe the venules

A

direct blood flow away from capillary bed

contain smooth muscle

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14
Q

What do precapillary sphincters do?

A

they are rings of smooth muscle that contract and relax to regulate blood flow into the capillary bed

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15
Q

What are cytokines?

A

the nervous system of the WBCs

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16
Q

What are chemokines?

A

the attract WBCs to a site

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17
Q

What happens if too much histamine is released? not enough?

A

too much causes hypersensitivity and not enough causes immunodeficiency

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18
Q

What are the 5 signs of inflammation?

A

redness, heat, swelling, pain, and loss of function

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19
Q

Define inflammation

A

the tissue response to injury or infection– occurs in vascularized tissue

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20
Q

Define inflammatory response

A

describes how various tissues react to injury or infection that causes tissue damage– non-specific, rapid response of injured tissue to any causative (etiological) agent of tissue damage

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21
Q

What are the purposes of the inflammatory response?

A

-limit further tissue damage
-prevent spread of injurious agent/infection
-stimulate adaptive immune response
-begin wound healing process

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22
Q

What effect does stromal tissue have on tissue damage?

A

-triggers the inflammatory response
-increases vascular permeability
-vasodilation
-fibroblasts secrete protein fibers called collagen
-mast cells secrete histamine and heparin

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23
Q

What does heparin do?

A

prevents blood clotting

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24
Q

What effect does parenchymal tissue have at the tissue damage site?

A

-may be damaged and need to be replaced
-do not directly cause the inflammatory response

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25
Q

What are the two patterns of inflammatory response and what determine which one it is?

A

1) acute inflammatory response
2) chronic inflammatory response

based on the duration of the response and the specific WBCs present in the lesion

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26
Q

Describe acute inflammation

A

-innate, immediate tissue response to injury
-main chemical mediator is 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 and macrophages (order is important)

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27
Q

Describe chronic inflammation

A

-innate and adaptive, prolonged tissue reaction to continued injury or persistent infection
-main chemical mediator is histamine
-still trying to limit the damage and promote wound healing, but scarring is probable
-predominant immune cells: macrophages, lymphocytes, and mast cells (order is important)

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28
Q

What are the 3 possible results of wound healing?

A

1) resolution– damaged cells recover
2) regeneration– replacement by same type of cell
3) repair– scarring occurs

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29
Q

What are the major WBCs involved in the acute inflammatory response and what do they do?

A

Mast cells– secrete histamine (major proinflammatory chemical mediator)

Neutrophils– phagocytic; first responders to tissue distress

Macrophages– phagocytic; clean up cellular debris (slow to get to the site)

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30
Q

What are the 3 types of plasma protein systems responses for the acute inflammatory response?

A

1) complement
2) coagulation
3) kinin cascades

These promote inflammation and blood clotting when needed

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31
Q

What are the 3 major components of the acute inflammatory response?

A

1) the vascular response

2) the cellular response

3) the plasma protein systems response

These are caused by the release of histamine and are all proinflammatory!

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32
Q

Describe the vascular response of the acute inflammatory response

A

the immediate histamine-mediated response by the microvascular endothelial and smooth muscle cells within the wound site; it will increase blood flow into the injured tissue and increase vascular permeability

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33
Q

Describe the cellular response of the acute inflammatory response

A

includes all 3 types of blood cells– WBCs, platelets, and RBCs as they respond to injured tissue and increase vascular permeability

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34
Q

Describe the plasma protein systems response of the acute inflammatory response

A

includes a variety of biochemical responses to injury; these proinflammatory proteins are part of the acute phase proteins, they are transported in the blood plasma to the injury site, where they act as proinflammatory mediators (complement system, coagulation system, and kinin system)

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35
Q

Where are mast cells located?

A

in the connective tissue surrounding the microvasculature

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36
Q

Where are histamine receptors located?

A

endothelial cells and smooth muscle cells

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37
Q

What are the effects of histamine release on the microvasculature during an inflammatory response?
(very long answer)

A

tissue damage stimulates mast cells to rapidly “degranulate” ie. release histamine from storage in cytoplasmic vesicles. Histamine bind to histamine receptors on vascular endothelial and smooth muscle cells causing specific independent responses and 3 things happen:
1) the arteriolar and precapillary sphincter smooth muscle cells-> histamine stimulates vascular smooth muscle cells to relax-> arteriole vasodilation and opens precapillary sphincters-> increased rate of blood flow to cap. bed

2) venular endothelium-> histamine stimulates endothelial cells to contract-> ‘myo’endothelial contraction creates inter-endothelial cell gaps-> increased vascular permeability

3) venular endothelium-> histamine also stimulates endothelial cells to decrease production of anti-endothelial cells and infiltrate the wound site-> promotes leukocyte infiltration and clot formation

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38
Q

What type of cells produce histamine?

A

Mast cells– 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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39
Q

What are the cell characteristics of mast cells?

A

-derived from pluripotent stem cells in red bone marrow
-reside in connective tissue (stromal immune surveillance cells)
-recognize tissue damage, microbial invasion

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40
Q

Describe the 2 mechanisms in which mast cells release proinflammatory mediators

A

1) mast cell degranulation
-immediate release of mediators
-the mediators are made in advance and stored in vesicles within the mast cell (look granular)
-histamine
-other proinflammatory mediators (chemotactic factors and cytokines)

2) mast cell synthesis
-slower release of newly synthesized mediators
-includes cell membrane components of damaged mast cells
-chemokines (made by any cell that is dying)

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41
Q

Does histamine cause pain?

A

not directly, it can stimulate the edema that pushed on nerve endings causing them to be compressed or irritated, it is said to elicit all 5 signs, even if one is an indirect effect

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42
Q

What is histamine?

A

a proinflammatory vasoactive amine that affects the microvasculature and other target tissue

basically means a chemical that causes a vessel to act/respond to stimulation by that chemical (vasoactive) and this chemical contains an NH2 (amine) group

43
Q

What are the 2 types of histamine receptors?

A

H1 receptors: proinflammatory effects on target cells
-endothelial cells
-vascular smooth muscle (makes it relax)
-bronchiole smooth muscle (makes this muscle constrict)
-immune cells (WBCs)

H2 receptors: anti-inflammatory effects on target cells
-gastric parietal (HCL secreting) cells (increase secretion)
-immune cells (WBCs)

44
Q

Antihistamines are antagonists to which type of histamine receptor?

A

H1

45
Q

What are some examples of drugs that are anti-inflammatory?

A

antihistamines, glucocorticoids, and NSAIDs

46
Q

What is the purpose of plasma?

A

-lubes the endothelial cells
-stops unwanted blood clots
-the reason cells go down the center of the vessel

47
Q

Describe blood flow in a 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

48
Q

Describe blood flow in acutely inflamed blood vessels

A

-histamine mediated ‘myo’endothelial cell contraction-> interendothelial cell gaps which then lead to:
-increased venular permeability
-endothelial cell secretion of pro-adhesion chemicals (CAMS)
-blood cells enter plasmatic zone-> adhere to endothelium-> enter wound site

results in edema

49
Q

What causes the 5 cardinal signs of inflammation?

A

histamine induced microvascular endothelial and smooth muscle responses to tissue damage

50
Q

What two types of microvascular cells respond to histamine?

A

endothelial and muscle cells

51
Q

What are the effects of histamine on the microvasculature?

A

a) in arterioles there is vasodilation (red and hot)
b) in capillaries there is passive vasodilation (red and hot)
c) in venules there is permeability (pain, edema, and loss of function)

52
Q

Why is the vascular response important during acute inflammation?

A

bring nutrients, protein, WBCs

53
Q

What are the clinical manifestations of the vascular response to histamine?

A

red, heat, swelling, pain, and loss of function

54
Q

What is actin’s normal function and which cells express actin?

A

motility and every cell if needed but normally endothelial and during inflammation WBCs

55
Q

Define edema

A

the excessive accumulation of fluid within the interstitial spaces

a tissue with excess fluid is called edematous

56
Q

How much excess tissue fluid needs to be present before the swelling becomes ‘noticeable’?

A

around 30%

57
Q

What is third spacing?

A

the fluid has entered the tissue (generalized edema)

58
Q

What is ascites?

A

abdominal-pelvic cavity has fluid

59
Q

What are the two types of edematous fluid?

A

1) transudate

2) exudate
-two subtypes are fluid exudate and cellular exudate

60
Q

What are the 4 pressures that control normal capillary exchange? and do they promote filtration or reabsorption?

A

1) Blood/capillary Hydrostatic Pressure (BHP)- filtration, pushes fluid out of capillaries into tissue
2) Interstitial Fluid Osmotic (Oncotic) Pressure (IFOP)- filtration
3) Blood/Capillary Osmotic (Oncotic) Pressure (BCOP)- reabsorption, pulls fluid into the capillaries from the tissue
4) Interstitial Fluid Hydrostatic Pressure (IFHP)- reabsorption

61
Q

How do the pressures change during an inflammatory response?

A

interstitial fluid pressure increases

62
Q

What is the difference between osmotic and oncotic pressure?

A

osmotic pressure is the pressure exerted by chemicals found in a solution that pull/attract water towards them (promote osmosis)– does not require a living membrane to occur

oncotic pressure is the osmotic pressure exerted by colloids in a biological solution, such as blood plasma or interstitial fluid

the terms are often used interchangeably

63
Q

Where is the highest fluid pressure and where is the lowest?

A

highest is in the arterioles and lowest is in the venules

64
Q

Describe the lymphatic system briefly

A

-drains into veins in neck
-absorbs excess interstitial fluid
-picks up 3L of fluid daily
-damaged in people with severe edema

65
Q

When the Blood Hydrostatic Pressure (BHP) goes up what happens?

A

arteriole vasodilation increases blood flow into capillary bed

66
Q

When the interstitial fluid osmotic pressure (IFOP) increases what happens?

A

presence of microbial proteins, cell debris, and proinflammatory mediators is tissue fluid

67
Q

When the blood colloid osmotic pressure (BCOP) decreases what happens?

A

normal: minimal effect

if liver disease: hypoalbuminemia

if kidney disease: proteinuria

68
Q

If the interstitial fluid hydrostatic pressure (IFHP) increases what happens?

A

arteriole vasodilation– increased venular vascular permeability and decreased lymphatic drainage

69
Q

Which direction is fluid movement during filtration? reabsorption?

A

filtration– into tissue

reabsorption– into blood

70
Q

What is the main difference between transudate and exudate?

A

timing of production and specific chemistry

71
Q

Describe transudate

A

-immediate, excess watery tissue fluid
-essentially the 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 pressure (due to arterial vasodilation)
-comes out of dilated arterioles

72
Q

Describe exudate– two types

A

1) fluid exudate– excess tissue fluid rich in plasma proteins (help with innate and adaptive immune response)

2) cellular exudate– includes the WBCs that infiltrate the injury site (in clotting, also includes platelets and RBCs)

-takes longer to begin as it requires myoendothelial contraction to occur
-comes out of venules because they have the biggest gaps

73
Q

Which form of edematous fluid is first to an injury site?

A

transudate

74
Q

What type of pressure causes edema?

A

an increase in Blood Hydrostatic Pressure (BHP) and decreased Blood Colloid Osmotic Pressure (BCOP)

75
Q

When a tissue is injured, 2 smooth muscle vascular effects occur in quick succession, what are they?

A

arteriolar vasospasm– immediate but brief contraction of vascular smooth muscle in response to sympathetic nervous system release of norepinephrine or epinephrine

arteriolar vasodilation– histamine mediated smooth muscle relaxation causing redness and heat

76
Q

Which cells promote inflammation?

A

-mast cells
-basophils
-neutrophils

77
Q

Which cells act as phagocytes?

A

-neutrophils
-macrophages
-dendritic cells
-B lymphocytes-> plasma cells
-NK cells
-eosinophils

78
Q

Which cells induce apoptosis?

A

-NK cells
-eosinophils
-cytotoxic T lymphocytes

79
Q

Which cell boosts innate and adaptive responses?

A

helper T cells

80
Q

What is pus made of?

A

dead and dying WBCs (mainly neutrophils), dead and dying body cells, and dead and dying bacteria

81
Q

What do WBCs respond to during acute inflammation

A

1) increased vascular permeability– causing slower local venule blood flow which allows WBCs to enter plasmatic zone and eventually produce cellular exudate

2) injured cell distress signals– cytokines and chemokines that promote WBC chemotaxis and infiltration into injury site

82
Q

Define chemotaxis

A

-the directional movement of leukocytes in response to a chemical gradient
-common chemotactic agents: cell debris, microbes, proinflammatory chemokines and cytokines

83
Q

Define margination

A

also called pavementation

mechanism by which WBCs move to outer margins of vessel (into plasmatic zone) tumble along the endothelium, and adhere to endothelium

84
Q

Define diapedesis

A

mechanism by which WBC squeeze into wound site through the inter-endothelial gaps

85
Q

What are CAMS?

A

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

86
Q

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

A

cellular

87
Q

Describe the platelet response during acute inflammation

A

occurs if the blood vessel wall is damaged during injury– are you bleeding?

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

88
Q

What is included in platelet activation?

A

platelet adherence-> platelet release reaction-> platelet plug formation-> hemostasis (meaning stop the bleeding)

89
Q

What are the components of a blood clot?

A

platelets, sticky fibrin threads and trapped RBCs

90
Q

Which NSAID blocks thromboxane A2 activity (during blood clotting)?

A

ASA/ aspirin–> blood thinner

91
Q

What do RBCs respond to during acute inflammation?

A

1) slower local blood flow
2) platelet activation

92
Q

What is included in RBC activation during acute inflammation?

A

RBC adherence-> rouleaux formation (stacked like coins)-> followed by extravasation (more bleeding).. bleeding into tissue-> RBCs help form extravascular blood clot

93
Q

What is the purpose of RBC response during acute inflammation?

A

to help limit blood loss by strengthening and stabilizing blood clot

94
Q

Describe the general characteristics of the 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
-act as proinflammatory mediators

they work by:
tissue damage-> inactive circulating proenzymes-> convert to active enzymes-> cascade of enzyme activity-> proinflammatory response

95
Q

Describe the complement system

A

-innate immune response
-series of 9 plasma proteins; called C1-C9
-come from the liver

96
Q

What is the mechanism of action of the complement system?

A

3 pathways of complement protein activation
1) classical pathway– antibody present
2) lectin pathway– bacteria present
3) alternative pathway– bacteria or yeast present

this is all you need to know about these pathways, they do not need to be memorized

97
Q

What are the functions of the complement system?

A

physiological effects of complement protein activation:
-form membrane attack complexes (MAC)
-act as opsonins
-act as leukocyte chemotactic agents
-act as anaphylatoxins
-attract antibodies to wound site

end result of complement activation is promote inflammation and help destroy pathogens

98
Q

Define opsonization (opsonin)

A

‘to make tasty’ 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

99
Q

What is the coagulation (blood clotting) system mechanism of action?

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 and RBCs and platelets get caught to form a blood clot

100
Q

What are the 2 routes to activation of the clotting cascade?

A

1) extrinsic– triggered by outside damage
-more common
-tissue damage stimulates parenchymal and stromal cells to release tissue factor

2) intrinsic– 99% pathology (starts in vessel)
-endothelial damage-> platelet-collagen interaction
-platelet activation

101
Q

Which cells break up bruises?

A

macrophages

102
Q

What gives a bruise its colour?

A

the breakdown of hemoglobin

103
Q

What enzyme breaks up blood clots by breaking down the fibrin threads?

A

plasmin– this process is called clot dissolution

pathophysiology 1 (5 decks)

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