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22 fall: path > Test 1: lecture 6 inflammation > Flashcards

Test 1: lecture 6 inflammation Flashcards

1
Q

3 main steps of inflammation

A

Vascular (stromal) responses

Migration and activation of leukocytes

Systemic reaction

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2
Q

5 signs of inflammation

A
  1. Rubor – redness
  2. Tumor – swelling
  3. Calor – heat
  4. Dolor – pain
  5. Functio laesa - Loss of function
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3
Q

Inflammation can cause further tissue damage and lead to healing by ___ or ___

A

REGENERATION

fibrosis (SCAR FORMATION)

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4
Q
A

phlebitis

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5
Q
A

fungal abomasitis

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6
Q

another name for redness

A

rubor

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7
Q

another name for swelling

A

tumor

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8
Q

another name for pain

A

dolor

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9
Q

another name for heat

A

calor

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10
Q

what are the two principle components of inflammation

A

Vascular reaction – involves fluid and plasma proteins (e.g. complement and fibrin), blood vessels, and extracellular matrix elements (increased blood flow and increased permeability)( vasodilation- NO, bradykinin,PGD2 permeability- histamine, bradykinin, PGE2, C5, C3, IL-1, TNF)

Cellular reaction – neutrophils, monocytes, eosinophils, lymphocytes, basophils, platelets, tissue mast cells, fibroblasts, and macrophages. Important role for extracellular matrix such as fibrous proteins (collagen and elastin) adhesive glycoproteins (fibronectin, laminin) and proteoglycans (movement of immune cells) chemotaxis- C5, IL-1, TNF

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11
Q

acute vs chronic inflammation

A

acute: rapid, short duration, neutrophils and edema

chronic: long, lymphocytes, macrophages, fibrous connective tissue and necrosis

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12
Q

what is the most important cell in acute inflammation

A

neutrophils

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13
Q

what are the most common cells during chronic inflammation

A

lymphocytes and macrophages

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14
Q
A

neutrophil

acute inflammation

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15
Q
A

monocyte which turns into a macrophage

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16
Q
A

lymphocyte -chronic inflammation

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17
Q

what kind of cells

A

Pleural fluid (exudate/vascular) from a dog with bacterial infection and pyothorax (what is pyothorax)

unhealthy neutrophils

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18
Q

how does histamine effect capillary blood flow

A

will vasodilate → increase blood flow (increase redness and heat)

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19
Q

4 steps of the vascular reaction on acute inflammation

A
  1. capillary blood flow increases (histamine, NO→ redness and heat))
  2. increased permeability of the vessel walls in the veins mostly (Starling relationship-bradykinin, histamine, C5, C3, PGE2)
  3. white blood cell and fluid leave the vessels = neutrophil emigration (tumor→ swelling-chemotaxis- IL-1 TNF)
  4. white blood cells are activated
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20
Q

____ and ___ are vasodilators

A

histamine and NO

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21
Q

increased blood flow causes which cardinal sign of inflammation

A

rubor- redness

calor- heat

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22
Q

During inflammation, blood flow ___and vessels ___and become permeable to vascular elements, allowing them to exit and enter sites of injury.

A

increases

dilate

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23
Q

increased vascular permeability is the cause of what cardinal sign

A

tumor- swelling

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24
Q

___ is increased blood flow

A

hyperemia

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25
Q

___ is the earliest manifestation of inflammation

A

Vasodilation

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26
Q

explain osmotic pressure

A

the pull of proteins to pull fluid back into the vessels

if proteins leak out there is less osmotic pressure and leads to a build up of fluid outside vessels → edema

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27
Q

explain hydrostatic pressure

A

the pressure to move things out of the vessel

opposite to osmotic pressure

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28
Q

histamine and bradykinin will cause ___ change their vascular permeability

A

HEV→ will cause gaps to form between vascular endothelium and allow fluid to leave

effects HEV in 15-30 mins, not capillaries and arterioles. those are effected 2-12 hours later by cytokines

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29
Q

journey from vessel lumen to interstitial tissue

A

Extravasation

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30
Q

the cellular reaction of inflammation involves what two steps

A

extravasation and phagocytosis

movement of cells out of the vessels and activation of cells to clean up

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31
Q

Normally RBC ’s form a central column and leukocytes are
displaced peripherally. Blood stasis and vessel dilation during inflammation produces greater leukocyte ___

A

margination

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32
Q

what causes rolling of leukocytes

A

selectins on the endothelium of blood vessels

sialyl-lewis X on the leukocyte

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33
Q

adhesion is by the ___ on the leukocyte and the ___ on the endothelium

A

integrins

ICAM and VCAM

b2 integrins (LFA-1 and Mac-1) bind ICAM-1
b1 integrins (VLA4) bind VCAM-1 (1o endo. adhesion molecule)
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34
Q

transmigration through the endothelium is by ____ on the endothelium and ___ on the leukocyte

A

PECAM

CD31

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35
Q

what are some things that can activate leukocytes

A

Arachidonic acid production

ysosomal enzyme production (degradative enzymes like
elastase and collagenase but also antibacterial such as
lysozyme and myeloperoxidase)

cytokine secretion

activation of adhesion molecules (integrins)

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36
Q

fluid, proteins, and blood cells that escape into interstitial spaces or the body cavities. Specific gravity > 1.020. caused by increased vascular permeability

A

exudate

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37
Q

suppurative exudate

A

pus

composed of neutrophils and dead cells (pus). Purulent is a synonym of suppurative. An abscess is a localized form of suppurative inflammation

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38
Q

Fibrinous exudate

A

increased vascular permeability during acute inflammation permits leakage of plasma proteins including fibrinogen, which is cleaved into fibrin and polymerizes into clots. This can occur in seconds.

Can later be replaced by fibrosis, which is a distinct process involving deposition of connective tissue by fibroblasts.

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39
Q

serous exudate

A

blister

fluid rich in protein on body surface → leakage from burns

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40
Q

exudate vs transudate

A

exudate → SG > 1.02 → contains proteins→ caused by increased vascular permeability

transudate→ SQ less then 1 → low protein content → caused by increased hydrostatic imbalances or a decrease in oncotic/osmotic pressure

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41
Q

transudate

A

fluid with low protein content (<1% albumen) with specific gravity < 1.012.

caused by an increased osmotic or hydrostatic imbalance across vessel wall or a decrease in colloid (oncotic) pressure w/o an increase in permeability of vessel wall.

ultrafiltrate of blood plasma

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42
Q

general term for increased fluid in the interstitium with the only exception being the LUNG where excessive fluid in the alveolar lumen is also defined as edema.

A

edema

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43
Q

fluid in the serous cavities

A

effusion

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44
Q
A

exudate

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45
Q

opsonination

A

prepare for eating

when a pathogen is coated in antibodies, complement or lectins and it makes it easier for the body to find and kill that pathogen

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46
Q

what enzyme is used by macrophages to kill bacteria

A

myeloperoxidase

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47
Q

within macrophages, myeloperoxidase makes hypochlorite (bleach) from ___. Most efficient killing system in neutrophils.

A

hydrogen
peroxide

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48
Q

Inflammatory mediators are produced by tissues and secreted into plasma (___ etc. must be activated) or produced locally by cells (___ etc.)

A

complement, kinins,

histamine, lysosomal enzymes,

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49
Q

list two Vasoactive amines (increase vascular permeability)

A

histamine

serotonin

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50
Q

Factor XIIa

A

hageman factor

starts the clotting pathway that leads to Fibrinogen (thrombin) → Fibrin

clot formation

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51
Q

Type 1 hypersensitivity pathway is by ___

A

mast cells, basophils and platelets produce histamine

causes arteriolar dilation, increase in venule permeability

principle mediator of immediate transient phase of
increased vascular permeability (endothelial H1 receptors)

52
Q

Histamine is produced primarily by ___

A

mast cells

53
Q

Complement system causes ___ vascular permeability, chemotaxis, & ___ pathogens.

A

increased

opsonizes

54
Q

3 pathways of complement

A
55
Q

3 outcomes of complement are

  • proteolytic fragments (C3a and C5a) ___ other cells
  • induction of microbe ___

___ by membrane attack complex (MAC)

A

activate→ inflammation

phagocytosis

cell lysis

56
Q

Fibrinogen (____) → Fibrin

A

Thrombin

57
Q

kinin system

A

breaksdown clots

plasmin is used to split fibrin

will produce bradykinin → cause pain

58
Q

what is a by product of the kinin system that causes pain

A

bradykinin

59
Q

what cardinal signs are caused by bradykinin

A

increase vascular permeability like histamine (tumor-swelling, calor-heat)

dilation of blood vessels (rubor-redness)

pain (dolor)

60
Q

____of clotting pathway is activated to XIIa by collagen, basement membranes, negatively charged surfaces.

A

Hagemann Factor (Factor XII

61
Q

___ converts prekallikrein to kallikrein, which converts plasminogen to plasmin, which lyses fibrin and activates C3.

A

Factor XIIa

62
Q

Interaction between clotting, inflammatory, complement and fibrinolytic systems by activated ___

A

Factor XIIa.

63
Q

pain is due to ___

A

bradykinin

64
Q

___ is found in triglyceride in the plasma membrane and is a lipid derived mediator

A

arachidonic acid

65
Q

___ are used to covert cell membrane to AA

A

phospholipases

steroid inhibit this step

66
Q

Cyclo-oxygenases (COX-1 and COX-2) convert AA into ___

A

prostaglandins, thromboxane, and prostacylines.

67
Q

prostacyclin (PGI2) cause ___

A

vasodilation, and inhibit platelet aggregation

arachidonic acid (COX1 and COX2) → PGG2 → prostaglandins, thromboxane, and prostacylines. (PGE2, PGD2, PGF2a, PGI2, TXA2

68
Q

prostaglandins cause

A

vasodilation and potentiate edema

arachidonic acid (COX1 and COX2) → PGG2 → prostaglandins, thromboxane, and prostacylines. (PGE2, PGD2, PGF2a, PGI2, TXA2

69
Q

Thromboxane cause ___

A

vasoconstriction, promote platelet aggregation

arachidonic acid (COX1 and COX2) → PGG2 → prostaglandins, thromboxane, and prostacylines. (PGE2, PGD2, PGF2a, PGI2, TXA2

70
Q

arachidonic acid (_____) → leukotrienes and lipoxins

A

5- lipoxygenase

71
Q

leukotrienes cause

A

vasoconstriction, bronchospasm and increased permeability

72
Q

Lipoxygenases produce ____from arachidonic acid

A

leukotrienes and lipoxins

73
Q

___ is Constitutively expressed - AA production for daily needs.

A

COX-1

74
Q

which pathway did Vioxx target

A

COX-2 caused cardiomyopathy

trying to prevent AA from turning into prostaglandins(vasodilation and edema), thromboxane (vasoconstriction and promote platelet clumping) , and prostacyline (vasodilation and inhibit platelets) that cause inflammation

75
Q

(aspirin and other NSAIDs lead to prolonged bleeding because they inhibit ___ production.)

A

TXA2 thromboxane

76
Q

PGI2

A

PGI2 (prostacylin) – from vascular endothelium, potent vasodilator,
inhibits coagulation, major product of endothelium.

77
Q

TXA2 – major product of ___. Causes platelet ____and
vaso___ , coagulation, is short lived

A

platelets

aggregation

constriction

78
Q

___ are involved in the pathogenesis of ASTHMA

A

LTC4, LTD4, LTE4 → cause vasoconstriction, bronchospasm and increased permeability

79
Q

LOX inhibitors

A

Used for asthma in cats and recurrent airway obstruction in horses)

May be useful in treatment of asthma where leukotrienes play a role
in pathogenesis (Fenleuron, Zileuton – 5 lipoxygenase inhibitor)
80
Q

how do steroid effect inflammation

A

decrease expression of genes encoding COX-2, PLA2 directly, IL-1,
TNF, and iNOS.

increase expression of anti-inflammatory genes, inhibit AA release from membranes.

81
Q

____ - major pro-inflammatory cytokines with systemic effects.

A

IL-1 and TNF

82
Q

IL-1 and TNF are produced by

A

activated macrophages

83
Q

what 4 effects do IL-1 and TNF have

A

acute-phase reactions

endothelial effects

fibroblast effects

leukocyte effects

84
Q

IL-1 and TNF released from leukocyte (macrophages), act as
pyrogens – increase COX activity and PG synthesis from ___

A

AA

85
Q

IL-1, IL-6, and TNF drive a 100 fold increase in production of key
liver proteins including: • C-reactive protein, fibrinogen, ___

A

serum amyloid A protein (SAA)

86
Q

Leukocytosis

A

IL-1 and TNF lead to an increase­ in the number of immature cells (left
shift) released from bone marrow.

87
Q

histamine and serotonin and made by ___ and cause a ___ in permeability

A

mast cells and platelets

+

88
Q

bradykinin are made by ___ and cause a ___ in permeability

A

plasma substrate (made by fibrin breakdown pathway)

+

pain

89
Q

___ is made by mast cells and causes Vasodilation, pain, fever

A

prostaglandins

90
Q

___ are made by macrophages and cause Acute-phase reactions, endothelial activation, fibroblast activation

A

IL-1 and TNF

91
Q

___ are made by macrophages and endothelium and cause vasodilation and cytotoxicity

A

nitric oxide

92
Q

outpouring of thin fluid.

A

serous effusion

93
Q

fibrinous inflammation

A

increased vascular permeability

fibrinogen leaves vessels and gets turned into fibrin

typical of body lining/cavity inflammation

94
Q

___ type of inflammation is common for the body lining/cavity

A

fibrinous

95
Q

____ is. typical of mucosal surfaces, exudate resulting from overproduction of mucus mixed with neutrophils and other leukocytes.

A

catarrhal inflammation

96
Q

suppurative inflammation

A

pus → neutrophils, necrotic cells, edema.

abscess

can be walled off

97
Q

3 outcomes of acute inflammation

A

complete resolution

healing by connective tissue replacement (fibrosis)

progression to chronic inflammation

98
Q

during complete resolution of acute inflammation what happens

A

vascular permeability normalized

edema reabsorbed

debris eaten

macrophages removed

99
Q

3 causes of chronic inflammation

A

persistent infection

exposure to toxin

autoimmunity

100
Q

___ are the dominant cells in chronic inflammation

A

Macs and lymphocytes

101
Q

Macrophages induce____ activation and proliferation (IL-1 and TNF), collagen deposition, and angiogenesis.

A

fibroblast

102
Q

Tissue ____ is one of the hallmarks of chronic inflammation.

A

destruction

103
Q

develop from activated B lymphocytes, produce antibody
against persistent antigen in the inflammatory site or against altered tissue components.

A

plasma cells

104
Q

activated by IgE in parasitic infections. ___ granules
contain major basic protein, which is toxic to parasites and mammalian epithelial cells.

A

eosinophils

Eosinophil

105
Q

____- widely distributed in connective tissues. Fc receptors bind
the Fc portion of IgE antibody. IgE antibodies bound to Fc receptors specifically recognize antigen, and the cells release mediators, such as histamine and products of AA oxidation.

A

mast cells

106
Q

two cell types that make up granuloma

A

epithelioid macrophage

multinucleated giant cell

107
Q

granulomas have ___ macrophages and ___ cells. They are also usually surrounded by ___ and are caused by ___

A

epithelioid macrophages

multinucleated giant cell

fibrosis

delayed type hypersensitivity (type 4)

108
Q

____ reactions are the driving cause of granulomas, i.e. this is a form of immunopathology

A

Delayed Type hypersensitivity (DTH) (Type 4 reaction)

109
Q

____ is an epithelioid macrophages forming granulomas with neutrophils in center of granuloma and pus

A

Pyogranulomatous inflammation

110
Q
A

granuloma

111
Q

List the five cardinal signs of inflammation and the underlying pathophysiological basis of each

A

Rubor – increased blood flow and tissue perfusion

b. Calor – increased blood flow and tissue perfursion
c. Dolor – bradykinin and other pain mediators, some prostaglandins and leukotrienes
d. Tumor – increased vascular permeability and fluid loss from vessels
e. Loss of function – tissue destruction, fibrosis, edema

112
Q

Conserved steps of Acute Inflammation

• Initiated by injury or agent, mast cells activated, tissue resident macrophages activated. ___blood flow due to ___

A

Increase

vasodilation.

113
Q

Neutrophils release cytokines (e.g. IL-1, TNF) and lipid mediators. IL-1 and TNF ____ vascular permeability and can have systemic effects (____)

A

increase

fever, nausea, malaise

114
Q

Know the difference between an exudate and a transudate. What are the key differences between these fluids and how is each formed?

A
  • *Exudate** – fluid, protein and cells that escape into interstitial spaces or the body cavities. Specific gravity > 1.020, high protein, mainly neutrophils
  • due to major increase in vascular permeability
  • *Transudate** – fluid with low protein content with specific gravity < 1.012
  • due to Increased hydrostatic (hypertension) imbalance across vessel wall or a decrease in colloid (oncotic - hypoproteinemia) pressure due to renal disease, burns, hepatic disease with decreased albumen production. Also seen in early acute inflammation. - ultrafiltrate of blood plasma
115
Q

____ is composed of neutrophils and dead cells (pus). example: An abscess

A

Suppurative exudate

116
Q

___ has increased vascular permeability during acute inflammation and accumulation of fluid with high protein and low cell numbers with S.G > 1.02. Associated with endothelial cell injury and leakage of larger MW proteins such as fibrinogen.

A

Fibrinous exudate

117
Q

___ are lesions characterized by accumulation of fluid rich in protein on body surfaces e.g. oozing of fluid from burns or Blisters

A

serous exudate

118
Q

___ is tissue response comprised of secretion or accumulation of thick
gelatinous fluid containing mucus from mucous membranes (goblet cells and mucous glands). Seen with allergic and chronic airway inflamation and autoimmune GI disease

A

catarrhal exudate

119
Q

___ cause expression of E-selectins on endothelium in 1-2 hours.

A

IL-1 and TNFa

120
Q

Cyclo-oxygenases (COX-1 and COX-2) convert AA into ___. Targets of NSAIDS, COX inhibitors, steroids.

A

• prostaglandins, thromboxane, and prostacylines. (PGE2, PGD2, • PGF2a, PGI2, TXA2).

121
Q

Lipoxygenases produce ___ from AA

A

leukotrienes and lipoxins

122
Q

Glucocorticoids decrease expression of genes encoding ___, IL-1, TNF, and iNOS.

A

COX-2, PLA2 directly

123
Q

Complement proteins orchestrate immune cell activation and pathogen killing by 3 main mechanisms. What are these mechanisms and which complement proteins/fragments are effectors of these mechanisms

A
124
Q

Phagocytosis – ___ are opsonins on bacteria and increase phagocytosis by neutrophils and macrophages

A

C3b and iC3b

125
Q

Myeloperoxidase makes ___ from hydrogen peroxide.

A

hypochlorite (bleach)

22 fall: path (46 decks)

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