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inflammation Flashcards

1
Q

triple response

A

a red scratch mark
red flare around the scratch mark
red swollen area (wheal) around the flare

dr. lewis found that he could eliminate the flare by cutting the autonomic nerve supply

this led to the discovery of histamine which mediates events 1 and 3

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2
Q

5 cardinal signs of inflammation

A 
Dolor (pain)
Calor (heat)
rubor (redness)
tumor (swelling)
functiolaesa (loss of function)
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3
Q

identifying plasma cell on slides

A

round oval nucleus pushed to one side b/c of large ER producing immunoglobulins

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4
Q

what are the stimuli for acute inflammation

A 
infections
necrotic tissues
hypoxia
foreign bodies
immune reactions
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5
Q

what happens to blood vessels during inflammation

A

vasodilation- greater blood flow (redness and heat)

vascular permeability–> leaky endothelial cells (histamine, bradykinin, leukotrienes)

exudation (fluid, proteins, red blood cells, WBC’s) due to increased hydrostatic pressure and increased osmotic pressure extravascularly

vascular stasis –> allows inflammatory cells to emigrate to site of injury

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6
Q

main mediators of vasodilation in inflammation (3)

A

prostaglandins (PGE2)
nitric oxide
histamine

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7
Q

main mediators of increased vascular permeability in inflammation (7)

A 
histamine
serotonin
C3a and C5a (by liberating vasoactive amines from mast cells)
Bradykinin
Leukotrienes C4, D4, E4
PAF
Substance P
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8
Q

what are the main mediators of chemotaxis, leukocyte recruitment and activation (7)

A 
TNF
IL-1
Chemokines 
C3a
C5a
Leukotriene B4
Bacterial products (n-formyl methyl peptides)
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9
Q

main mediators of fever (3)

A

IL1
TNF
Prostaglandins (PGE2)

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10
Q

main mediators of pain 2

A

prostaglandins

bradykinin***

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11
Q

main mediators of tissue damage in inflammation 3

A

lysosomal enzymes of leukocytes
ROS
NO

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12
Q

what mediates increased transcytosis

A

VEGF

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13
Q

what happens to lymph vessels during inflammation

A

they proliferate due to increased load of fluid (Edema)

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14
Q

lymphangitis

A

inflammation of the lymphatics

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15
Q

lymphadenitits

A

inflammed lymph nodes and vessels

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16
Q

adenitis

A

infammation of lymph nodes

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17
Q

what is edema

A

excess fluid in interstitial or serous spaces (can be exudate or transudate)

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18
Q 
transudate 
why is it formed
protein content?
color?
consistency
odor?
ph
cell count
enzyme content
bacteria
inflammation
A

ultra filtrate of plasma that leaks due to increased hydrostatic pressure or decreased colloid osmotic pressure (decreased protein synthesis –> liver disease or increased protein loss –> kidney disease)

low protein content

clear/water-like 
thin and watery
no odor
Alkaline
low cell count
low enzyme content
no bacteria
no inflammation present
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19
Q

exudate
why does it form?

color
consistency
odor?
ph?
protein content?
cell count?
enzyme content?
bacteria?
inflammation?
A

mix of cells and plasma leaking out of vessels in response to chemical mediators

cloudy, white, yellow or red
thick and creamy,
may have odor
acidic 
high protein content
high cell count (WBC and RBC)
high enzyme content
bacteria may be present
associated with inflammation
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20
Q

serous

A

yellow to clear

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21
Q

serosanguinous

A

clear with red tinge

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22
Q

sanguionous

A

full of blood

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23
Q

purulent

A

greenish (full of neutrophils)

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24
Q

chylous

A

milky and white

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25
Q

what is the immediate transient response

A

immediate response with almost any stimulus
leakage starts with injury (lasts 15-30 min)
endothelial cells contract

driven by histamine, bradykinin, serotonin, leukotrienes, substance P

no neutrophils
mostly venules affected

ex. dermatographism

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26
Q

what is the immediate sustained response

A

severe thermal or chemical burns or lytic bacterial infection

leakage starts with injury and last several hours to days

venules, capillaries, arterioles affected

endothelial cell necrosis !!

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27
Q

what is the delayed prolonged leakage

A

patient develops inflammation
leakage starts 2-12 hours AFTER injury

lasts hours to days

bacterial toxins, sun burn,

capillaries and venules affected

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28
Q

what are the steps in leukocyte migration?

A

stasis - slowing of blood
margination- white cells move to periphery
rolling- weak binding via selectins
adhesion/activation - integrin activation by chemokines and firm adhesion by integrins
migration - diapedesis across endothelial cells (must express collagenase for type IV collagen)

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29
Q

what are 3 selectins

and what controls the expression of selectins and their ligands

A

L -selectin- expressed on leukocytes
E - selectin - expressed on endothelial cells
P -selectin - one in platelets and on endothelium

expression of selectins and their ligands is regulated by cytokines produced in response to infection and injury (TNF, IL-1 released by macrophages)

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30
Q

ICAM-1

A

intercellular adhesion molecule 1 provides more firm adhesion of the neutrophil, via integrins on neutrophil surfaces, to the endothelium.

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31
Q

CD31

A

this cell to cell adhesion molecule aids in diapedesis.

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32
Q

what is the role of IL-8, C5a and LTB4 after deapedesis

A

chemotaxis is aided by the C5a component from complement activation, along with leukotriene B4, a product of the lipo-oxygenase pathway of arachidonic acid metabolism.

these cause increases in Ca2+ and kinases which leads to polymerization of actin ==> filipodia move in direction of inflammatory stimulus

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33
Q

what is the role of • C3b and IgG

A

opsonins such as the C3b component from complement activation, as well as immunoglobulin G, coat foreign objects such as bacteria to aid in phagocytosis by binding to leukocyte receptors.

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34
Q

where are weibel - pallade bodies

A

in endothelial cells - they are the intracellular stores of P =selectin

when there is inflammation hisatmine and thrombin upregulate and resdistribute Pselectin to surface of endothelial cell

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35
Q

what are the exogenous chemotactic factors

A

bacterial formyl-peptides

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36
Q

what are the 4 major types of receptors on leukocytes ?

A

TLR’s–> for microbial products
G- protein coupled receptors –> for Lipid mediators, chemokines, and for N-formyl methionyl peptides
Cytokine receptors–> IFN-gamma is the major cytokine that activates macrophages

Receptors for opsonins (proteins that coat microbes which includes antibodies, complement, lectins, etc).

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37
Q

G- protein coupled receptor activation on leukocytes leads to …

A

cytoskeletal changes and signal transduction:
chemotaxis–> migration into tissues
increased integrin avidity–> adhesion to endothelium

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38
Q

TLR’s activation on leukocytes leads to what

A

production of mediators (AA metabolites and cytokines) –> amplication of the inflammatory reaction

production of ROS and lysosomal enzymes —> killing of microbes

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39
Q

Cytokine receptor activation leads to what

A

production of ROS and lysosomal enzymes –> killing of microbes

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40
Q

activation of phagocytic receptor on leukocytes leads to what…

A

phagocytosis of microbe into phagosome

production of ROS and lysosomal enyzmes –> killing of microbes

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41
Q 
Chediak higashi syndrome
gene?
outcome of mutated gene?
symptoms
peripheral smear
treatment
A

autosomal recessive
LYST gene malfuntion

defective fusion of phagosomes and lysosomes in phagocytes

symtpoms:
albino b/c melanin made in melanocytes can't get to the keratinocytes 
recurrent infections 
progressive neurological abnormalities 
coagulation defects 
plasma membrane repair impaired

peripheral smear shows:
giant cytoplasmic granules in leukocytes and platelets
neutrophils that have giant azurophilic granules

treatment
hematopoietic cell transplantation

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42
Q

chronic granulomatous disease

x-linked
autosomal recessive

A

defects in bacterial killing and oxidative burst
results from inherited defects in genes encoding components of phagocte oxidase

x-linked - phagocyte oxidase membrane compoenet
autosomal recessive - phagocyte oxidase cytoplasmic component

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43
Q

bone marrow suppression?

A

defective production of leukocytes

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44
Q

MPO deficiency

A

decreased microbial killing because of defective MPO-H2O2 system

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45
Q

what are the cell derived mediators of inflammation that are preformed 2

A

histamine

serotonin

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46
Q

what are the cell derived mediators of inflammation that are newly synthesized 6

A 
prostaglandins
leukotrienes
PAF
ROS
NO
Cytokines
chemokines 
substance P
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47
Q

what are the plasma derived mediators of inflammation

A 
complement products (C5a, C3a)
Kinins (bradykinin)
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48
Q

what releases histamine 3

A

basophils
platelets
mast cells

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49
Q

what are the actions of histamine

A

binds H1 receptors on endothelial cells

causes:
constriction of large arteries
dilation of arterioles
increased venular permeability via endothelial cell contraction

bronchial and intestinal smooth muscle contraction
induces nasal and bronchial mucus secretion
activates sensory nerves (itching)

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50
Q

what is the source of serotonin

what is its release triggered by

A

present in platelets

released when platelets aggregate after contact with collagen, thrombin, adenosine diphosphate, antigen/antibody complex

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51
Q

what are the effects of serotonin

A

vasodilation

increased vascular permeability

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52
Q

action of phospholipase A2

A

converts cell membrane phospholipids to arachidonic acid

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53
Q

cyclooxgenase general function

A

converts AA to prostaglandins

includes COX1 and COX2

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54
Q

5-lipoxygenase function

A

converts AA to leukotrienes and lipoxins

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55
Q

what cells produce prostaglandins

A

mast cells
macrophages
endothelial cells

56
Q

COX1

A 
constitutively active
produces TXA2 (thromboxane)
57
Q

Cox2

A

inducible

produces prostacyclin PGI2

58
Q

Thromboxane A2
what is it produced by?
function?

A

produced by platelets (b/c platelets contain thromboxane synthetase)

causes platelet aggregation and vasoconstriction

59
Q

prostacycline (PGI2) function

produced by what?

A

produced by endothelium (b/c endothelium contains prostacyclin synthetase)

inhibits platelet aggregation and causes vasodilation

60
Q

PGD2

A

attracts neutrophils
vasodilation
pain and fever (via cAMP action on temp set point)

61
Q

PGE2

A

cuases pain

vasodilation

62
Q

PGF2

A

vasodilation

63
Q

leukotrienes function?

A

increased vascular permeability
chemotaxis
leukocyte adhesion and activation

64
Q

LTB4

A

attracts leukocytes

65
Q

LTC4, D4, E4

A

cause vasoconstriction
increased vascular permeability
bronchoconstriction (bronchospasm)

66
Q

lipoxins

A

inhibit leukocyte recruitment and inflammation

67
Q

function of Cox 2 inhibitors

A

impair endothelial cell production of prostacyclin (which is a vasodilatro and inhibitor of platelet aggregation

side effects>
increased risk of cardiovascular and cerebrovascular events b/c there is now unopposed COx-1 which is a vasoconstrictor and inducer of platelet aggregation

68
Q

lipoxygenase inhibitors

A

inhibits production or blocks receptors of 5 -lipoxygenase

note NSAIDs do not affect 5-lipoxygenase
used in the treatment of asthma

69
Q

broad spectrum inhibitors

A

including steroids

reduced gene transcription of COX2 , phospholipase A2 and pro-inflammatory cytokines (IL-1 and TNF) and INOS

70
Q

PAF
made by what
causes what?

A

made by platelets, endothelial cells and leukocytes

causes platelet aggregation
vasoconstriction and bronchoconstriction
enhanced leukocyte adherence to endothelium (integrin mediated leukocyte binding)

with very low concentrations it causes vasodilation and increased vascular permeability

71
Q

ROS in inflammation

A

cause endothelial cell damage with resultant increased vascular permeability

damage to parenchyma cells and erythrocytes

inactivates proteases such as alpha-antitrypsin (normally inhibits elastase)

72
Q

NO in inflammation

A

relaxes smooth m. and promotes vasodilation

inhibits leukocyte rolling, adhesions, degranulation

inhibits platelet aggregation and adhesion

inhibits mast cell activated inflammation

endogenous mechanism for preventing inflammation ***

73
Q

what are the three types of NO and how is their activity increased?

A

eNOS - endothelial
nNOS- neuronal
iNOS- inducible when monocytes and macrophages are activated by TNF and INF

74
Q

which cytokines are important in acute inflammation

A

TNF
IL-1
IL-6
Chemokines

75
Q

which cytokines are responsible in chronic inflammation

A

IL-12
IFN-gamma
IL-17

76
Q

IL-1
what controls its production
what are its functions

what happens in mutations that activate caspases of inflammasome

A

production controlled by inflammasome

causes endothelial activation (endothelial adhesion, acute phase response, fever, activates fibroblasts and neutrophils)

increased active IL-1 with mutations that activate caspases of infalmmasome causing inherited autinflammatory syndromes (Mediterranean fever)

77
Q

TNF functions

A

regulates energy balance - promotes lipid and protein mobilization and suppresses appetite–> cachexia ***

Expression of luekocyte adhesion molecules

procoagulant

leukocyte activation

fever, leukocytosis, increase sleep

78
Q

substance P

A

mast cell activation and wheal formation
prominent in GI tract and lungs

causes:
pain
endocrine cell activation
mast cell activation
vascular permeability 
anti-vasopressor activity
79
Q

hageman factor (XII) is activated by what?

A

negatively charged surfaces:

  • when vascular permeability increases and plasma proteins leak into the extravascular space and come into contact with collagen
  • comes in contact with BM exposed as a result of endothelial cell damage

it is produced in the liver

80
Q

hageman factor stimulates what?

A

kinin system–> produces vasoactive kinins (bradykinin)
clotting system–> induces formation of thrombin
fibrinolytic system–> produces plasmin
complement system –> produces anaphylatoxins and other mediators

81
Q

kinin system activation by XII

what are the functions of kallikrein

A

XII converts prekallikrein to kallikrein

kallikrein converts HMWK to bradykinin
kallikrein makes C5 into C5a
Kallikrein converts plasminogen to plasmin
kallikrein also feedsback and activates more XII

82
Q

what are the functions of plasmin

A

converts C3 to C3a

cleaves fibrin into fibrin-split products (inflammation by chemotatic for leukocytes and increased vascular permeability)

83
Q

what activates thrombin

what are the functions of thrombin

A

thrombin is activated by XII as it activates teh clotting cascade

thrombin converts fibrinogen to fibrin

84
Q

what is the fibrinolytic system

A

XII activates this system by production of kallikrein

kallikrein then activates plasminogen to plasmin

this system counterbalances clotting because plasmin cleaves fibrin

plasmin also cleaves the complement protein C3 to produce C3a

plasmin also activates hageman factor amplifying the cascades

85
Q

what are the functions of bradykinin

A

increases vascular permeability
contraction of smooth muscle
dilation of blood vessels
PAIN ***

86
Q

classically activated macrophages respond to what?

A

respond to microbial products (TLR ligands)

respond to T cell cytokines (IFN- gamma)

87
Q

what are the products of classically activated macrophages

A

ROS
NO
Lysosomal enzymes

IL-1, IL-12, IL-23
chemokines

88
Q

what are the functions of classically activated macrophages

A

microbicidal actions
phagocytosis and killing of many bacteria and fungi

pathologic inflammation

89
Q

what do alternatively activated macrophages respond to

A

cytokines such as IL-4 and IL-13 (Th2 subset t cell products)

helminths

90
Q

what are the products of alternatively activated macrophages

A

IL-10
TGF-beta

Arginase
proline polyaminases

91
Q

what are the functions of alternatively activated macrophages

A

anti-inflammatory
wound repair
fibrosis

92
Q

what makes the MAC

A

C5b-C9

93
Q

anaphylatoxins in the complement cascades

A

C3 a , C4a, C5a
‘
cause histamine release and increase vascular permeability

94
Q

C5a function

A

leukocyte activation
chemotaxis
lipoxygenase

95
Q

C3b

A

opsonin - promotes phagocytosis

96
Q

what is the most critical step in the complement cascade

A

proteolysis of the third component C3

97
Q

what are the outcomes of acute inflammation

A 
resolution
pus formation (abscess) 
healing to fibrosis
chronic inflammation (angiogenesis, mononuclear cell infiltrate, fibrosis, progressive tissue injury)
98
Q

what does an elevated CRP mean

A

when elevated it can be a sign of a patient that is at increased risk of developing MI from atherosclerosis

it is an acute phase reactant and anytime there is inflammation this is elevated

99
Q

what are diseases that are from acute leukocyte induced injury

A

acute respiratory distress syndrome (neutrophils)
acute transplant rejection (lymphocytes, antibodies and complement)

asthma (eosinophils, IgE antibodies)

glomerulonephritis (neutrophils, monocytes, antibodies and complement)

septic shock (cytokines)

lung abscess (neutrophils)

100
Q

what are some disease that are involved in chronic leukocyte - induced injury

A

arthritis (lymphocytes, macrophages, antibodies)

asthma (eosinophils, IgE antibodies)

Atherosclerosis (macrophages)

chronic transplant rejection (lymphocytes and cytokines)

pulmonary fibrosis (macrophages, fibroblasts)

101
Q

what are active ways that the acute process is ended

A

switch in AA products to lipoxins

liberation of anti-inflammatory cytokines (IL-10 and TGF-Beta)

production of anti-inflammatory lipid mediators (resolvins and protectins) derives from polyunsaturated fatty acids (fish-oil)

neural changes (cholinergic discharge) - decrease TNF production by macrophages

102
Q

what are the acute morphological patterns of inflammation

exudative vs. necrotizing

A

exudative

  • serous (urticarial- itching)
  • fibrinous - protein rich
  • fibrinoid
  • hemorrhagic
  • catarrhal- common cold/snot (neutrophils and proteins)
  • purulent/suppartive (neutrophils)
    a. cellulitis
    b. lymphangitic
    c. abscess
    d. ulcerative
    e. pseudo-membranous

necrotizing
-wet gangrene

103
Q

morphological patterns of chronic inflammation

A

granulomatous

104
Q

disease associatred with abscess

A

multiple bacterial absecess in the lung in the case of bronchopneumonia

105
Q

what are two examples of pseudomembranous inflammation processes

what is the morphological appearance

A

c difficilecolitis

c diptheriae pharyngitis

form of exudative inflammation that involves mucous and serous membranes

fibrin in the exudate causes a membrane-like covering that is fairly adherent to the underlying acutely inflamed tissue

106
Q

what is an example of fibrinous inflammation

appearance?

A

fibrinous pericarditis
endocarditis

large molecules such as fibrinogen pass the vascular barrier and fibrin is formed and deposited in the extracellular space

107
Q

what is an ulcer

acute stage versus chronic stage

A

a local defect or excavation of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflamed necrotic tissue

can only occur when tissue necrosis and resultant inflammation exist on a near surface

108
Q

what is an abscess

A

large amounts of pus or puruluent exudate consisting of neutrophils, liquefactive necrosis, edema fluid

abscesses are localized collections of purulent infllammatory tissues caused by suppuration buried in a tissue

they have a central region that appears as a mass of necrotic leukocytes and tissue cells

there is a zone of preserved neutrophils around this necrotic focus

outside this region vascular dilation and parenchymal and fibroblastic proliferation occur indicating chronic inflammation and repair

in time the abscess may be walled off and replaced by connective tissue

109
Q

what are the causes of chronic inflammation

A

continued infections (delayed type hypersensitivity) and sometimes this takes a specific pattern called granulomatous reaction

prolonged exposure to toxic/foreign agents

autoimmune diseases (RA, MS, inflammatory bowel, allergic)

malignancies

110
Q

what are morphological characteristics of chronic inflammation

A

mononuclear cell infiltrates (macrophages, lymphocytes, plasma cells, basophils, mast cells, eosinophils)

tissue destruction

fibrosis

proliferation of blood vessels

111
Q

if you get an acute viral infection what goes up in the peripheral blood that is not usually norma l and is an exception

A

lymphocytes increase instead of neutrophils

112
Q 
macrophages in the ....
liver
spleen and lymph nodes
lungs
central nervous system
bone
skin
A 
kupffer cells
sinus histiocytes
alveolar macrophages
microglia
osteoclasts
langerhan cells (antigen presenting)
113
Q

what is the main cell type in chronic inflammation and what is its function

A

macrophage

products of activated macrophages serve to eliminate injurious agents such as microbes, and to initiate the process of repair

responsible for tissue injury in chronic inflammation (proteases, ROS)

114
Q

what is the relationship b/w t cells and macrophages and what cytokines are involved

A

activated T cells produce
1) cytokines that recruit macrophages (TNF, IL-17, chemokines)

2) cytokines that activate macrophages (IFN-gamma)

Activated macrophages in turn stimulate T cells by presenting antigens and by secreting cytokines (IL-12)

115
Q

what cytokine regulates eosinophils

what are the chemoattractants for eosinophils?

what do eosinophils look like on a slide?

A

produced in the BM and regulated by IL-3 and IL-5 and GM-CSF

chemoattractants include eotaxin 1 and 2
RANTES

on a slide the eosinophils have little red granules, 1-2 lobes

116
Q

what are the constituents of eosinophil granules

A

major basic protein –> toxic to some parasites and causes lysis of mammalian epithelial cells - necrosis

cytotoxic agents (cationic proteins, neurotoxin, peroxidase)

the only parasite touched by eosinophils are helminths

117
Q

basophils in chronic granulation

A

circulating leukocytes with large basophilic granules containing histamine and heparin

118
Q

what is the function of heparin

A

contained in basophils and acts as an anticoagulant

119
Q

mast cells in chronic inflammation

A

wildely distributed in connective tissue
have receptors for Fc portion of IgE molecules
upon stimulation by recognition of antigen –> they degranulate and release mediators such as histamine (itching and vasodilation)

120
Q

what immunolglobulin activates mast cells

A

IgE

121
Q

what cytokine is an important mediator of granulmoatous inflammation

A

INF-gamma

transforms macrophages into epitheloid cells

122
Q

what is granulamtous inflammation

A

microscopic aggregate of activated macrophages that are transformed into epithelium-like cells surrounded by a collar of mononuclear leukocytes, principally lymphocytes and occasionally plasma cells

123
Q

tuberculosis granuloma on stain shows what

A

an area of central necrosis surrounded by multiple lagerhan’s type giant cells
epitheloid cells
lymphocytes

124
Q

foreign body granuloma

A

sutures, talc

dont incite any specific inflammatory immune response

foreign material in the center of the granuloma

macrophages, collagen, few small lymphocytes, multinucleated giant cells

125
Q

immune granulomas

A

inciting agent produces immune response

macrophages engulf foreign protein antigen , process and present to T cell

T cells produce IL-2 and IFN-gamma which activates more macrophages –> converted into mutlinucleate giant cells

mycobacterium tuberculosis is an example

126
Q

what are diseases that are examples of diseases with granulomatous inflammation

A 
tuberculosis
leprosy
syphilis
cat-scratch disease
sarcoidosis 
crohn's disease
127
Q

what is a fever caused by?

what cytokines mediate a fever?

what are the systemic manifestations of fever

A

produced in respones to pyrogens whcih stimulate prostaglandin synthesis in vascular and perivascular cells of the hypothalamus

exogenous pyrogens (bacterial products (LPS) stimulate leukocytes to release cytokines

cytokines are endogenous pyrogens that increase enzymes that convert AA into prostaglandins

Cytokines:
IL-1, TNF, IL-6, Interferon

systemic outcomes:
sympathetic NS stimulation
dermal vasoconstriction
decreased heat dissipation

128
Q

what are the acute phase proteins

A

CRP
fibrinogen–> binds to red cells and causes them to form stacks (rouleaux)

serum amyloid A (SAA protein)

129
Q

what is the problem with elevated hepcidin in the blood (which is produced in the acute phase response)

A

reduces the availability of iron and are responsible for the anemia associated with chronic inflammation

130
Q

what occurs in sepsis

A

large amounts of bacteria and LPS

generates large amounts of cytokines (TNF and IL-1)

activation of coagulation and fibrinolysis (blood clots and then massive bleeding)

=end organ damage

  • cardiac failure and vasodilation (NO production) –> decrease in BP

adult acute resp. distress syndrome

131
Q

what is the cause of chronic granulomatous disease

A

characterized by reduced killing of ingested microbes b/c of inherited defects in NADPH oxidase system

132
Q

what diseases cause deficiency in chemotaxis

A 
thermal injury
DM 
malignancy
sepsis 
immunodeficiency
133
Q

what diseases cause adhesion deficiencies

A

hemodialysis

DM

134
Q

what diseases cause phagocytosis and microbicidal activity deficiencies

A 
leukemia 
anemia
sepsis 
DM
neonates
malnutrition
135
Q

neutrophil adherence molecule defects are caused by what diseases

A 
hereditary
glucocorticoids
dm
ethanol
recurrent bacterial infections

PBD (7 decks)

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