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PATHOLOGY > INFLAMMATION PT. 1 > Flashcards

INFLAMMATION PT. 1 Flashcards

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1
Q

Inflammation

A

host response to injury or insult due to: infection, trauma, toxins, loss of blood, vaccination

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2
Q

Stimulus for inflammation cascade

A

pathogen or necrotic tissue

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3
Q

Sentinel cells

A

cells that recognize the pathogen or necrotic tissue and produce mediators in response (stimulus for inflammation); otherwise remain inactive waiting to see if anything goes awry

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4
Q

Examples of sentinel cells

A

dendritic cells, macrophages and mast cells

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5
Q

Mediators

A

released products from sentinel cells to regulate inflammatory response; have a direct effect on the response

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6
Q

Examples of mediators

A

cytokines, amines

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7
Q

Acute inflammation

A

up to 7 days

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8
Q

Sub-acute inflammation

A

7-30 days

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9
Q

Chronic inflammation

A

more than 30 days

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10
Q

Most common Agranulocyte

A

lymphocyte

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11
Q

B- cells

A

lymphocytes that mature in the bone marrow; they become plasma cells to secrete antibodies

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12
Q

Natural killer (NK) cells

A

lymphocytes that naturally kill virally infected/damaged cells; part of the innate immune system since they do not need to be taught how to do this

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13
Q

T-cells

A

lymphocytes that mature in the thymus; respond to specific antigens on APCs

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14
Q

γδ T-cells

A

T- lymphocytes with a limited range of receptors; a RESTRICTED type of T-cell

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15
Q

CD4+ T-helper cells

A

secrete cytokines that promote inflammation and influence the nature of the inflammatory reactions; help other cells promote immune function

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16
Q

Th1

A

secretes pro-inflammatory cytokines like TNF, IL-1, IL-6 and interferon gamma (IFN-γ) which activates macrophages via classical pathway; involved in defense against many types of bacteria and viruses and in the chronic inflammation seen in many autoimmune diseases

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17
Q

Th2

A

CD4+ T-helper cell that secretes IL-4, IL-5, and IL-13, which recruit and activate eosinophils and are responsible for the alternative pathway of macrophage activation; important in defense against helminthic parasites and in allergic inflammation

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18
Q

Th17

A

CD4+ T-helper cell that secretes IL-17 and other cytokines, which induce the secretion of chemokines responsible for recruiting mainly neutrophils; involved in defense against many types of bacteria and viruses and in the chronic inflammation seen in many autoimmune diseases

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19
Q

CD8+ Cytotoxic T- cells

A

kill virally infected cells and cancer cells

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20
Q

M1 macrophage

A

produces pro-inflammatory cytokines and chemokines; also produces reactive oxygen species, NO, lysosomal enzymes to phagocytize and kill INGESTED bacteria and fungi; is CLASSICALLY activated

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21
Q

M2 macrophage

A

produces anti-inflammatory cytokines to promote wound repair, healing and fibrosis
- secrete growth factors that promote angiogenesis, activate fibroblasts, and stimulate collagen synthesis

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22
Q

Macrophages are immature until…

A

… they are exposed to a pathogen

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23
Q

Humoral immunity

A

B cells differentiate into plasma B cells to produce antibodies against a specific antigen; deals with antigens from EXTRACELLULAR pathogens
- antibodies will bind to antigens, neutralize them, cause lysis or phagocytize
- quicker to act

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24
Q

Cellular immunity

A

targets INTRACELLULAR pathogens and is mediated by T lymphocytes;
- pathogen’s antigens are expressed on the cell surface or on an antigen-presenting cell
- helper T-cells release cytokines that help activated T cells bind to the infected cells’ MHC-antigen complex and differentiate the T cell into a cytotoxic T cell & the infected cell then undergoes lysis
- takes longer to recruit

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25
Acute inflammation molecules can be..
cell derived or plasma protein derived
26
Cell derived inflammation molecules (mediators)
are either pre-formed in storage as granules or made de novo in the cell i.e: histamine, cytokines, prostaglandins
27
Plasma derived inflammation molecules (mediators)
exist as inactive proteins already circulating in the blood and are produced by the liver i.e: complement proteins and kinins
28
Histamine
sources: mast cells, basophils, platelets actions: vasodilation, increased vascular permeability, endothelial activation stimuli for release: physical injury, binding antibodies to mast cells, fragments of complement C3a, C5a
29
Prostaglandins
sources: mast cells, WBCs actions: vasodilation, pain, fever - is an arachidonic metabolite
30
Leukotrienes
sources: mast cells, WBCs actions: increased vascular permeability, chemotaxis, WBC adhesion and activation - is an arachidonic metabolite
31
Cytokines
sources: macrophages, mast cells, endothelial cells actions: endothelial activation, fever, hypotension
32
platelet activating factor
sources: WBCs, mast cells actions: vasodilation (at low levels), increased vascular permeability, WBC adhesion, chemotaxis, degranulation, oxidative burst, platelet aggregation,
33
chemokines
sources: WBCs, activated macrophages actions: chemotaxis, WBC activation
34
Complement proteins
sources: plasma actions: WBC chemotaxis and activation, vasodilation, direct killing
35
Kinins
sources: plasma actions: vasodilation, increased vascular permeability, smooth muscle contraction, pain
36
Neutrophils
lifespan of <2 days in the blood and sites of inflammation; do NOT recirculate --> they migrate to the injury site and stay there and die there
37
steps of acute inflammation
1- blood vessel changes to increase flow 2- microvascular changes (i.e vasodilation) to allow proteins and cells to leave the blood 3- emigration, accumulation and activation of WBCs
38
hyperemia
dilation of blood vessels to increase blood flow; dilation typically of the arterioles as they have a smooth muscle layer (elastin component) that can stretch to accommodate changes in flow
39
Properties of inflammatory mediators
- are continuously made - stimulate other cells to release secondary effector molecules or to amplify or oppose a given response - are quickly destroyed/removed as time and space are limited
40
serotonin
cell- derived mediator
41
Earliest mediators
histamine and serotonin (cells have already made them so they can be immediately released)
42
Nitric oxide (NO)
vasodilator that relaxed smooth muscle; involved in bacterial killing
43
Biologically active proteins
made from larger, inactive precursors that undergo proteolytic cleavage to become active i.e- complement proteins, insulin, coagulation proteins
44
Bradykinin
source: plasma actions: increased vascular permeability, smooth muscle contraction, vasodilation, pain
45
TNF
pro-inflammatory cytokine that stimulates expression of endothelial adhesion molecules and secretion of other cytokines - has systemic effects; also causes fever - source: macrophages, mast cells, T-cells
46
IL-1
- pro-inflammatory cytokine similar to TNF - has larger role in fever - source: macrophages, endothelial cells
47
IL-6
pro-inflammatory cytokine with an acute response - has systemic effects - source: macrophages, mast cells, T cells, most cells with a nucleus
48
chemokines
chemoattractant cytokines that are secreted by many cells at sites of inflammation - bind to endothelial cell proteoglycans and are displayed at high concentrations on the endothelial surface - activate & recruit WBCs to site of inflammation and lymphocytes to lymph nodes - source: macrophages, mast cells, T cells
49
complement proteins
soluble proteins and their receptors that help antibodies defend against pathogens - undergo necessary proteolytic cleavage to become active and amplify immune response - activated in 3 ways
50
Alternative pathway
triggered by microbial surface molecules (e.g., endotoxin, or lipopolysaccharide [LPS]), complex polysaccharides, and other substances, in the absence of antibody
51
Classical pathway
triggered by fixation of C1 to antibody (IgM or IgG) that has combined with antigen
52
Lectin pathway
plasma mannose-binding lectin binds to carbohydrates on microbes and activates C1, also without a role for antibody
53
C5a and C3a complement proteins
effector function: INFLAMMATION - recruitment and activation of leukocytes --> destruction of microbes by leukocytes - are anaphylatoxins that release histamine from mast cells --> vasodilation and increased vascular permeability
54
C3b complement protein
effector function: PHAGOCYTOSIS - recognized by C3b receptor --> phagocytoses microbe, coating(opsonization) the microbe so it can be marked for destruction
55
C5a
56
MAC
effector function: CELL LYSIS --> lysis of microbe
57
Transudate
fluid that passes due to hydrodynamic forces or early in the inflammatory response; has a LOW concentration of cells and protein - essentially an ultrafiltrate of blood plasma that is produced as a result of osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability and is usually not associated with inflammation
58
Exudate
fluid that escapes from the vasculature, typically as a result of inflammation; has a HIGH concentration of cells and protein - presence implies that there is an increase in the permeability of small blood vessels, typically during an inflammatory reaction
59
Effusion
escape of fluid into defined cavity; can be exudate or transudate; can be drained with a needle
60
Edema
accumulation of fluid into the interstitial space of tissues or alveolus; can be exudate or transudate
61
Serous exudate
clear fluid containing few cells and many proteins - presence suggests mild vascular injury - i.e a skin blister
62
Purulent exudate
contains many inflammatory cells, mainly neutrophils - "pus"
63
Hemorrhagic exudate
contains many red blood cells - presence implies capillary damage
64
Fibrinous exudate
contains a layer of fibrin deposited onto the serosal surface - i.e bread and butter pericarditis
65
Process of leukocyte migration across vessel wall
1- margination when vasodilation occurs 2- rolling adhesion via selectins 3- tight adhesion via integrins of the vessel wall 4- migration across the vessel wall
66
Pulmonary edema
buildup of protein rich fluid in the lungs
67
Selectins
rolling adhesion molecules for leukocytes - i.e P- selectins
68
Integrins
tight adhesion molecules for leukocytes to adhere, arrest and then migrate out of the blood vessel - i.e ICAM-1
69
chemotactic factors for neutrophils
IL-8 CXC chemokines, C5a, bacterial products, platelet activating factor, leukotriene B4 LTB4 - all factors that influence neutrophil recruitment to the site of inflammation
70
Purpose of adhesion molecules
to foster close contact between adaptive immune cells; are also important in the migration of T and B cells in specific areas in the lymph nodes
71
Fever
cytokines (IL-1, TNF) acting upon the hypothalamic center of the brain, inducing pyrogens to elevate body temperature usually by 1° to 4°C - bacterial products such as LPS stimulate leukocytes to release the cytokines IL-1 and TNF, which upregulate the production of prostaglandins, particular PGE 2 , in the vascular and perivascular cells of the hypothalamus - PGE 2 elevates the body’s temperature by altering the firing of neurons in the preoptic nucleus of the hypothalamus - one of the most prominent manifestations of the systemic response
72
How to reduce fever?
Inhibit prostaglandin synthesis
73
Leukocytosis
increased release of leukocytes from the bone marrow promoted by colony stimulating factors - common feature of inflammatory reactions especially those induced by bacterial infections - leukocyte count usually climbs to 15,000 or 20,000 cells/μL
74
Leukemoid reactions
extreme event where leukocyte count may reach extraordinarily high levels of 40,000 to 100,000 cells/μL, resembling tat of leukemia
75
Acute phase response/reactants
consists of the production of plasma proteins, in which their levels in the blood may increase up to several hundred-fold as part of the response to inflammatory stimuli - synthesis in the liver stimulated by cytokines (i.e IL-6) -
76
Acute phase proteins
serum proteins stimulated by cytokines that must leave the blood and enter the tissue to the site of inflammation to mediate reaction - i.e C-reactive protein (CRP), fibrinogen, serum amyloid A (SAA)
77
CRP
C-reactive protein - binds to microbial cell walls and may have roles in host defense by acting as opsonins and by fixing complement
78
SAA
serum amyloid-A - binds to microbial cell walls and may have roles in host defense by acting as opsonins and by fixing complement
79
Fibrinogen
neutralizes the negative surface charge of red cells, causing them to form stacks of cells (called rouleaux ) that sediment more rapidly at unit gravity than do single red cells - basis for measuring the erythrocyte sedimentation rate as a simple test for detecting inflammation
80
Vascular leak
allows for the removal of necrotic tissue from the blood
81
Ways of bacterial killing
1- extracellular traps 2- intracellular killing by phagocytosis, engulfment and killing/degradations
82
Neutrophil Extracellular Traps (NETs)
Product of a dying neutrophil that expels its chromatin and proteins to trap the bacteria/pathogen - these proteins have microbial properties that will kill the pathogen
83

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