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FMS Week 8 (also some 7) Immunology > Intro to Inflammation > Flashcards

Intro to Inflammation Flashcards

(71 cards)

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1
Q

Inflammation

A

the response of vascularized tissues to infections and damage that brings cells and molecules of host defense from circulation to the sites where they are needed to eliminate offending agents (and repair damaged tissues)

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2
Q

Causes of acute inflammation

A

1) infection
2) physical injury (cuts, burns)
3) Foreign bodies (splinters, sutures)
4) Immune reaction (allergy, hypersensativity)

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3
Q

Acute inflammation steps

A

local tissue damage

vasodilation

erythema (rubor)

increase in temp (calor)

Increased capillary permeability, fluid accumulation (edema, pain)

continues chemotaxis

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4
Q

Edema

A
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5
Q

Neutrophils

A

Active phagocytes in tissue

Attracted to tissue by chemotactic factors such as complement, clotting proteins

Kill by ROS, granule contents

Release interleukin 8 (a chemokine that attracts inflamm response)

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6
Q

Macrophage

A

Ingest microbes and damaged cells

Produce IL-6, TNF-α, and IL-1

Produce growth factors that aid in repair

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7
Q
A

Neutrophil

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8
Q
A

Macrophage

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9
Q

Leukocyte responses

A

Note that there are different receptos. Release of cytokines when microbe binds leads to amplification of inflamm response

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10
Q

Macrophage effector function

A

Macrophage can either be involved in repair or inflammation and tissue injury

For repair it releases growth factors (platelet derived and fibroblast gf)

In inflammaiton they release ROS and nitrogen species

also release chemokines

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11
Q

Inflammatory cytokines funciton to

A

mobilize neutrophils

activate the vascular endothelium

chemotactic

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12
Q

On sensing microbial products, macrophages secrete a variety of pro-inflammatory cytokines

A

IL6
Fever. Induces acute-phase protein production by hepatocytes

TNF-α
Avtivates vasculat endothelium and increases vascular permeability, which leads to increased entry of complement anc cells to tissues and increased fluid drainage to lymph nodes.
Causes fever. Mobilization of metabolites. Shock.

IL-1ß
Activates vascular endothelium. Activates lymphocytes. Local tissue destruction. Increases access of effector cells.
Causes fever, production of IL-6.

CXCL8 (IL-8)
Chemotactic factor recruits neutrophils and basophils to site of infection

IL-12
Activated NK cells

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13
Q

IL 6

A

Fever

Induces acute phase protein production by hepatocytes

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14
Q

TNF-α

A

Activates vascular endothelium and increases vascular permeability, which leadds to increased entry of complement and cells to tissues and increased fluid drainage to lymph nodes

Fever

Mobilization of metabolites

Shock

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15
Q

IL-1ß

A

Activates vascular endothelium

Activates lymphocytes

Local tissue destruction

Increaes access of effector cells

Fever

Production of IL-6

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16
Q

CXCL8 (IL8)

A

Chemotactic factor recruits neutrophils and basophils to site of infection

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17
Q

IL12

A

Activates NK cells

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18
Q

Acute phase proteins

A

IL-1 IL-6 and TNF go to liver

Liver makes:
Fibrinogen
Serum amyloid A
C reactive protein
C3
Haptoglobin

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19
Q

Eosinophils release

A

cytokines and chemokines

leukotrienes

prostaglandins

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20
Q

Basophils release

A

histamine

heparin

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21
Q

Mast cells release

A

Histamine

TNF-α in allergic response and pathogen invasion

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22
Q
A

Eosinophils

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23
Q
A

Basophils

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24
Q
A

Mast cells

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25
Histamine leads to
Blood clots Gastric acid secretion Blood vessels to dialate Bronchoconstriction Increased permeability of capillaries Adrenaline release Swelling and inflammation Frequent heart beat
26
Endothelium
Express adhesion molecules for leukocutes Increased by TNF-α and IL-1 Proliferate during inflammation to handle increased flow Produce proinflammatory cytokines and to induce chemotaxis and stimulate angiogenesis for tissue repair
27
Leukocyte migration
Cytokines can up regulate selectins which allow leukocutes to slow down, roll, and enter ECM
28
Chemotaxis
Chemical signals that cause immune cells to migrate to a site of infection or injuty There is a chemotactic gradient. Brings immune cells to site and causes migration into tissues
29
Vasodilation and vascular permeability
The redness and heat of inflammation Vasodilation happens- immune cells and proteins can leak into tissue
30
Nitric Oxide
Macrophages produce this. NO leads to reduced leukocyte adhesion to vessel wall Vascular smooth muscle relaxation and vasodilation Reduced adhesion of platelets
31
Vasodilators
Nitric oxide histamine prostaglandins serotonin
32
Macrophages produce what vasodilator
Nitric oxide
33
What cells produce histamine vasodilator
Basophils and mast cells
34
What cells produce prostaglandins
eosinophils and endothelial cells
35
Endothelial cells
36
Vascular permeability through histamine release
Basophils and mast cells
37
Vascular permeability through leukotrienes
eosinophils and endothelial cells
38
Vascular permeability through bradykinin
endothelial cells
39
Vascular permeability can happen through release of
histamine leukotrienes bradykinin complement components
40
Arachadonic acid
important in vasodilation and vascular permeability cyclooxegenase can turn a acid into prostoglandins Cox 1, COX 2, ASA, and indomethacin can inhibit this Steroids inhibit phospholipids from being turned into arachadonic acid
41
Clotting
Sometimes good thing needed to stop bleeding. Can wall off infection. Platelets critical. Cytokines produced by macrophaged cause dilation of local small blood vessels Leukocytes move to periphery of blood vessel as a result of increased expression of adhesion molecules Leukocytes extrqavasate at site of infection Blood clotting occurs in the microvessels
42
Platelets
Contribute to blood clots Release: ROS to recruit additional platelets Fibroblast growth factors for wound repair Serotonin for vasodilaiton Anti-microbial peptides
43
Platelets
44
Clotting and repair
Clotting in A is good. Bacteria contained locally. Can not escape.This can happen if we inhibit plasminogen In B, plasminogen leads to clot dissolution and you have bacteria spreading. This can lead to larger infection.
45
Kinins and clotting cascades
Kininn cascade Bradykinin can lead to vascular permeability Thrombin can turn fibrinogen into fibrin plasmin can also lead to fibrin
46
D dimer
measure of fibrin degradation products
47
Prothrombin time
time in secronds for a fibrin clot to form
48
Clinical coagulation tests
When you have a clot there is some fibrin involved. As a result of this when you have clotting you can get fibrin degradation products Prothrombin time is ther time in seconds that it takes a fibrin clot to form D dimer is measure of fibrin degredation products
49
Mediators of vasodilation (to increase blood flow to site of the infection)
histamine nitric oxide prostaglandins
50
Mediators of vascular permeability (helping immune cells to get to tissues)
Histamine complement bradykinin leukotrienes
51
Mediator of chemotaxis
IL-8 Chemokines Complement
52
Mediators of fever
TNF-α IL-1 IL6 Prostaglandins
53
Mediators of pain
prostaglandins bradykinin
54
Mediators of tissue damage
ROS NO
55
Morphologic patterns of acute inflammation- serous
Skin blister from burns or viral infection leads to accumulation of fluid
56
Morphologic patterns of acute inflammation- fibrinous
Continues vascular permeability - fibrinogen influx
57
Morphologic patterns of acute inflammation- purulent
Abcess cavity containing neutrophils and cellular debris surrounded by congested blood vessels Liquefactive necrosis
58
Ulcer
An ulcer is formed by shedding of inflamed necrotic tissue of: Mouth Stomach Intestines Genitals
59
Sepsis
Systemic inflammation Amplified whole body inflammatory response to trauma/infection cytokine strom destorys tissues Systemic inflammatory response syndrome (SIRS) due to infection Multiple organ dysfunction syndrome (MODS)
60
Systemic inflammation Local inflammation
Endothelial cells. TNF and IL-1 signal. chemokines made Increased permeability of cells Leukocytes signaled by TNF and IL-1 Produce IL-1 IL-6 and chemokines
61
Systemic inflammation Systemic protective effects
TNF-α, IL-1 , and IL-6 signal brain. Leads to fever. IL-1 and IL6 signal liver. Leads to acute phase proteins. TNF, IL-1, and IL-of 6 signal bone marrow. Leukocyte production
62
Systemic inflammtion Systemic pathological effects
TNF signals heart. Low cardiac output. TNF signals endothelial cells/ blood vessels Thrombus. Increased permeability TNF signals skeletal muscle. Insulin resistance.
63
Resolution of inflammation
Injury can happen and inflammtion happens. Vascular changes, Neutrophil recruitment. Limited tissue injury. Resolution can happen. We want this. Back to normal function. However, we can get fibrosis or chronic inflammation which can be bad. Fibrosis is collagen deposition and loss of function.
64
Chronic inflammation causes
Persistant infections (ex TB, H pylori) Immune mediated diseases autoimminity, allergic diseases Prolonges exposure to toxic agents Cancer
65
Cells in chronic inflammation
Activated macrophages help activate T cells TNF and IL-17, and chemokines lead to reccruitment of neutrophils and macrophages. Inflammation. Activation of macrophages can again activate T cells through antigen presentation to T cells
66
Graulomas
morphological manifestation of chronic inflammation Aggregation of T cells and macrophages to contain an offending agent that is difficult to eradicate
67
Atherosclerosis
Endothelial damage Fatty streak formation- contains lipid filled macrophages (foam cells) and activated T cells Fibrous cap- advanced stage to wall off lesion Plaque rupture- material inside plaque released, thrombus occurs Treated by statins- decreased leukoccyte adhesion and NO, inhibits cholesterol synthesis
68
Inflammatory bowel disease
Ulcerative colitis and crohns disease persistant immine response to normal fluora activated macrophages and CD4+ T cells sectere cytokines, prostaglandins, leukotrienes, NO Characterized by diarrhea, rectal bleeding, and weight loss Increased risk for colorectal cancer
69
Overview of inflammation
70
Inflammatory cytokines promote cancer
71
Acute vs Chronic Inflammation Causative agent Major cells involved Primary mediators Onset Duration Outcomes

FMS Week 8 (also some 7) Immunology (9 decks)

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