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

Intro to Inflammation Flashcards

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
Q

Histamine leads to

A

Blood clots

Gastric acid secretion

Blood vessels to dialate

Bronchoconstriction

Increased permeability of capillaries

Adrenaline release

Swelling and inflammation

Frequent heart beat

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26
Q

Endothelium

A

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

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27
Q

Leukocyte migration

A

Cytokines can up regulate selectins which allow leukocutes to slow down, roll, and enter ECM

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28
Q

Chemotaxis

A

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

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29
Q

Vasodilation and vascular permeability

A

The redness and heat of inflammation

Vasodilation happens- immune cells and proteins can leak into tissue

30
Q

Nitric Oxide

A

Macrophages produce this.

NO leads to reduced leukocyte adhesion to vessel wall

Vascular smooth muscle relaxation and vasodilation

Reduced adhesion of platelets

31
Q

Vasodilators

A

Nitric oxide

histamine

prostaglandins

serotonin

32
Q

Macrophages produce what vasodilator

A

Nitric oxide

33
Q

What cells produce histamine vasodilator

A

Basophils and mast cells

34
Q

What cells produce prostaglandins

A

eosinophils and endothelial cells

35
Q
A

Endothelial cells

36
Q

Vascular permeability through histamine release

A

Basophils and mast cells

37
Q

Vascular permeability through leukotrienes

A

eosinophils and endothelial cells

38
Q

Vascular permeability through bradykinin

A

endothelial cells

39
Q

Vascular permeability can happen through release of

A

histamine

leukotrienes

bradykinin

complement components

40
Q

Arachadonic acid

A

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
Q

Clotting

A

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
Q

Platelets

A

Contribute to blood clots

Release:
ROS to recruit additional platelets
Fibroblast growth factors for wound repair
Serotonin for vasodilaiton
Anti-microbial peptides

43
Q
A

Platelets

44
Q

Clotting and repair

A

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
Q

Kinins and clotting cascades

A

Kininn cascade
Bradykinin can lead to vascular permeability

Thrombin can turn fibrinogen into fibrin plasmin can also lead to fibrin

46
Q

D dimer

A

measure of fibrin degradation products

47
Q

Prothrombin time

A

time in secronds for a fibrin clot to form

48
Q

Clinical coagulation tests

A

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
Q

Mediators of vasodilation

(to increase blood flow to site of the infection)

A

histamine

nitric oxide

prostaglandins

50
Q

Mediators of vascular permeability

(helping immune cells to get to tissues)

A

Histamine

complement

bradykinin

leukotrienes

51
Q

Mediator of chemotaxis

A

IL-8

Chemokines

Complement

52
Q

Mediators of fever

A

TNF-α

IL-1

IL6

Prostaglandins

53
Q

Mediators of pain

A

prostaglandins

bradykinin

54
Q

Mediators of tissue damage

A

ROS

NO

55
Q

Morphologic patterns of acute inflammation- serous

A

Skin blister from burns or viral infection leads to accumulation of fluid

56
Q

Morphologic patterns of acute inflammation- fibrinous

A

Continues vascular permeability - fibrinogen influx

57
Q

Morphologic patterns of acute inflammation- purulent

A

Abcess cavity containing neutrophils and cellular debris surrounded by congested blood vessels

Liquefactive necrosis

58
Q

Ulcer

A

An ulcer is formed by shedding of inflamed necrotic tissue of:

Mouth

Stomach

Intestines

Genitals

59
Q

Sepsis

A

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
Q

Systemic inflammation

Local inflammation

A

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
Q

Systemic inflammation

Systemic protective effects

A

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
Q

Systemic inflammtion

Systemic pathological effects

A

TNF signals heart. Low cardiac output.

TNF signals endothelial cells/ blood vessels
Thrombus. Increased permeability

TNF signals skeletal muscle. Insulin resistance.

63
Q

Resolution of inflammation

A

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
Q

Chronic inflammation causes

A

Persistant infections (ex TB, H pylori)

Immune mediated diseases
autoimminity, allergic diseases

Prolonges exposure to toxic agents

Cancer

65
Q

Cells in chronic inflammation

A

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
Q

Graulomas

A

morphological manifestation of chronic inflammation

Aggregation of T cells and macrophages to contain an offending agent that is difficult to eradicate

67
Q

Atherosclerosis

A

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
Q

Inflammatory bowel disease

A

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
Q
A

Overview of inflammation

70
Q
A

Inflammatory cytokines promote cancer

71
Q

Acute vs Chronic Inflammation

Causative agent

Major cells involved

Primary mediators

Onset

Duration

Outcomes

A

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

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