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Hannah MOD > chapter 3: inflammation > Flashcards

chapter 3: inflammation Flashcards

1
Q

describe the formation of granulomas (tubercles)

A

MO MHC2 CD4+ cell presentation—> MO secretion of IL-12 –>induce TH1 cell type–>IFNY release –> formation of M1 epitheliod histiocytes and giant cells –> more IL-12 secretion to continue the cycle

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2
Q

what is proud flesh

A

excess granulation tissue that need to be removed for proper scar formation

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3
Q

describe the process of adhesion

A

binding of neutrophilic integrins to CAMs on the endothelium

integrins upregulated by C5a and LTB4
CAMs unregulated by TNF and IL-1

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4
Q

what are the 3 general phases of acute inflammation

A
  1. fluid phase (swelling from dilation and increase vascular permability)
  2. neutrophil phase (recruitment of neutrophils)
  3. Macrophage phase (activation of consequential response of repair or adaptive immunity)
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5
Q

describe the process of transmigration/diapidesis

A
  • occurs in post capillary venule

- uses PECAM-1 (CD31) intracellular adhesion molecule to transmigrate through the endothelium

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6
Q

what does TH1 cells secrete

A

IL-2 for CD8+ t cell growth/activation

IFN-Y for MO M1 activation

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7
Q

cytokines that induce vasodilation

A

histamine
serotonin
PGI2/ D2/ E2

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8
Q

what are the chemotactants the recruit neutrophils in chemotaxis

A

IL-8
LTB4
C5a
bacterial products

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9
Q

source and function of histamine

A

mast cells, basophils, platelets

-dilation, increased permeability, endothelial activation (p-selection release)

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10
Q

function and source of IL-12

A

APCs (macrophages, dendritic cells)

stimulate TH1 cell type to increase IFN production

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11
Q

what type of inflammation associated with chronic inflammation and what are the hallmarks

A

granulomateous

  • epitheloid histiocytes with pink cytoplasm
  • multi-nucleated giant cells with lymphocyte rims
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12
Q

ECM deposition depends on a balance of what factors

A

TGF - fibrogenic agent
MMP - ECM degradation
TIMPS - MMP inhibitor

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13
Q

cytokines that induce pain

A

bradykinin

PGE2

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14
Q

what are the components of ECM

A

collagen
lamnin
proteoglycans
fibroblasts

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15
Q

source of kinins and complement

A

plasma produced in liver

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16
Q

what is the left shift

A

seen in luekocytosis of the acute phase response

-when huge increase in neutrophils initially causes subsequent increase in immature neutrophils in blood

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17
Q

secretion of M2 and function

A

TGF-B and GF = tissue repair and fibrosis

IL-10 and TGF-B = anti-inflammatory

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18
Q

describe how fever is caused in an inflammatory response

A

IL-1 and TNF travel to the perivasculature of the hypothalamus and subsequently increase COX activity which produces PGE2 which induces an increase in set point of body temperature

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19
Q

what are the 5 R’s of inflammatory reaction

A
  1. recognition
  2. recruitment
  3. removal of pathogen
  4. regulation of response
  5. repair
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20
Q

which APPs are activated by IL-6 and opsonize comeplement and clear necrotic cells

A

CRP and fibrinogen

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21
Q

cytokines that induce fever

A

IL-1
TNF
PGE2

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22
Q

what are the morphologic patterns of acute inflammation

A

serous
fibrinous
ulcer
purulent (suppurative)

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23
Q

what does TH2 secrete

A 
IL-4 = IgG/E class switching 
IL-5= eosinophil activation, IgA switching 
IL-10 = inhibits TH1, anti inflammatory 
IL-13 = M2 activation
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24
Q

what causes activation of CD4+ tcells and what is its function

A

MHCII APC presentation of extracellular antigen = binding of B7 (on APC) to CD28 (on t-cell)

TH1 = M1 MO activation, CD8+ T cell activation

TH2= helps B cell activation, and M2 MO activation

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25
Q

what pharmacological agents can be used asthma treatment

A
  1. lipooxgenase inhibitor
    - inhibit bronchospasm effects of Its
  2. LT antagonist
    * NSAIDs don’t affect lipoogenases or Its
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26
Q

what are the mediators that induce P-selectin release from webel palade bodies

A

histamine and thrombin

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27
Q

what is fibrinous acute inflammation pattern

A

inflammation of the lining of body cavities causes leakage of proteins such as fibrinogen (a procoagulant) leading to FIBROUS EXUDATE
-can lead to fibrosis if extensive leakage with activation
“bread and butter pericarditis”

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28
Q

which growth factor is responsible for endothelial proliferation ? angiogenesis ?

A

proliferation
VEGF

angiogenesis
FGF

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29
Q

define dehiscence

A

wound opening

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30
Q

define pus

A

a purulent inflammatory exudate rich in dead neutrophils and other WBCs and microbe debris

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31
Q

what is the process of regeneration and repair

A 
regeneration = uninjured cell proliferation and stem cell maturation 
repair= deposition of new connective tissue
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32
Q

what condition is associated with C1 inhibitors of complement

A
  • Block C1 activation in classic pathway

- hereditary angioedema

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33
Q

function of DAF and CD59 and what disease is associated with it

A

DAF-prevents C3 converstase function
CD59 prevents MAC formation

both are anchored by GPI and GPI deficiency = paroxysmal nocturnal hemoglobinuria

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34
Q

source of TNF

A

macrophages
mast cells
T-cells

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35
Q

what process of wound healing is responsible for some edema

A

angiogenesis

bc vasodilation by VEGF

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36
Q

describe the process of rolling

A

a component of neutrophil membrane (sialyl lewis X) will bind to selectins on endothelial wall and causing slowing of neutrophil movement

  • P-selectins are induced by histamine and thrombin release on webel-palade bodies
  • E-selectins and L-selectins are upregulated by TNF and IL-1
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37
Q

define hypertrophic scar

A

excess T1 collagen = large scar

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38
Q

what are the types of stimuli that cause an inflammatory reaction

A

microbial infection
tissue necrosis (from cell injury)
foreign bodies
immune reaction (hypersensitivity run from allergies or autoimmune)

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39
Q

describe oxygen dependent phagocytic killing

A

ROS
-O2–(NADPH oxidase)–> O2- —(SOD)—> H202—(MPO)–> HOCL

NO
-Arginine —(iNOS)—> NO
NO converts O2- –>ONOO- (peroxynitrate)
NO causes vasodilation

40
Q

corticosteroid inhibit what

A

gene transcription of Cycloogenases (COX) and lipooxygenases
-decreases LTs and PGs which affects inflammation

41
Q

describe the 3 step process of phagocytosis induced by neutrophils in acute inflammation

A
  1. recognition
    - requires neutrophil activation by phagocytic receptor microbial recognition (mannose receptor and scaveneger receptor), increased intracellular Ca2+, and protein kinase C and phospholipase A2 activation.
  2. vacuole engulfment extension of pseudopod that engulfs microbe into phagosome. phagosome combines with lysosome to make phagolysosome
  3. killing by phagolysosome
    - O2 dependent (ROS or NO)
    - O2 independent (lysosomal enzymes)

*enhanced by opsonins (MBL, C3b, IgG)

42
Q

how does thrombin activate the inflammatory response

A

intiate the release of P-selectins which induces activation of endothelium

43
Q

source and function of IFN-Y

A

acute inflammation
T-cells
-macrophage and neutrophil recruitment

chronic
T-cells and NK cells
-activate MO killing function

*stimulated by IL-12 from macrophages

44
Q

what are the phagocytic opsonins

A

(MBL, C3b, IgG)

45
Q

define keloid

A

excess T3 collagen = large scar

46
Q

macrophages kill by what mechanism of phagocytosis

A

O2 independent killing (lysozyme)

47
Q

what do macrophages release for WBC recruitment and inflammation

A

TNF

IL-1

48
Q

source and function of IL-6

A

macrophages

-acute phase response

49
Q

which PG is prostacyclin and what is its function

A

PGI2 = prostacyclin

  • inhibits platelet aggregation (opposite of TXA2)
  • vasodilation and increased permeability
50
Q

what is septic shock? and what is it caused by?

A

caused by pathogens and increased IL-1 / TNF

hypotensive stoke
intracellular coagulation (DIC) 
metabolic dysfunction (hyperglycemia)
51
Q

details of the last step of scar formation

A
  • ECM protein deposition

- T3 —> T1 collagen by collagnease and zinc cofactor

52
Q

what are the cardinal signs of inflammation

A 
redness (rudor)
warmth  (calor) 
swelling (tumor) 
pain (dolor) 
-fever

*loss of function

53
Q

function of mast cells

A

FCeRI binds to FC receptor of IgE and induces release of histamine and PGs for pro-inflammatory response

54
Q

what is the purulent acute inflammation pattern

A

pus exudate (dead neutrophils)
-associated with abscess and bacterial infection of pyogenic bacteria(
(-seen with staph and liquefactive necrosis )

55
Q

_____ kill by ROS species using phagocytic receptors

A

granulocytes

*MPO is a granule

56
Q

what is the oxidative burst of phagocytic killing

A

conversion of O2 to O2- by NADPH oxidase

57
Q

what are the steps in scar formation

A
  1. MO M2 clear debris and secrete GF and TGF-B for fibroblast migration and proliferation
  2. angiogenesis
  3. deposition of CT
    i. granulation tissue - fibroblast proliferation
    ii. scar formation - ECM deposition
58
Q

function of TGF-B

A
  • fibroblast migration/ chemotaxis
  • ECM protein production/ deposition
  • anti-inflammatory
59
Q

what are the 3 steps in the acute phase response ? and what is it induced by ?

A
  1. fever (induced by endogenous and exogenous pyrogens)
  2. acute phase protein release
  3. leukocytosis (extreme increase in WBC )

*induced by TNF, IL-1, IL-6

60
Q

what induces M1 formation? M2 formation ?

A

M1

  • IFN-Y from Tcells
  • microbes

M2

  • IL-4
  • IL-5
  • IL-13
61
Q

function of IL-1

A

fever
adhesion (upreg selectins and CAMs)
Th17 activation for acute inflammation

62
Q

function of TNF

A

adhesion (upreg E selections and CAMs)
decreasing appetite (other local and systemic effects)
WBC activation
fever

63
Q

what are the steps in neutrophil recruitment

A
  1. margination
  2. rolling
  3. adhesion
  4. diapedesis
  5. chemotaxis
    * phagocytosis follows
64
Q

what are the 3 fibroblast chemotactants

A

TGF-B
FGF
PDGF

65
Q

sources of IL-1

A

macrophages
mast cells
endothelial cells

66
Q

extent of cell injury in acute vs chronic inflammation

A

acute
-mild-self-limited tissue injury

chronic
-severe, progressive tissue injury

67
Q

what is the ulcer acute inflammation pattern

A

sloughing of dead necrotic tissue due to decreased blood supply to area
(seen in T1DM)

68
Q

what cytokine is a big component of creating the warmth, redness, and swelling seen in acute inflammation

A

histamine

69
Q

what are the types of collagen and associated tissues

A 
*from most strong to least 
1- bone 
2- cartilage 
3-BVs, granulation tissue
4- basement membrane
70
Q

describe B-cell maturation / activation process

A

immature B-cell–>naive B cell (IgM/IgD) –>activation by Ag binding and plasma cell production of more Cells; APC MHCII presentation and CD40 CD40L binding

*use IL-4/5 for isotype switching

71
Q

what are the three possible outcomes of acute inflammation

A
  1. complete resolution (regeneration)
  2. healing repaid by connective tissue replacement (scarring)
  3. chronic inflammation
72
Q

what are the acute phase (plasma) proteins increased in the acute phase response

A

CRP
fibrinogen
serum amyloid A
hepcidin

*made in the liver!

73
Q

what is serous acute inflammation pattern

A
  • exudation of TRANSUDATE into body cavities

ex: asitces

74
Q

describe the process of margination

A

WBCs move from center of blood vessel to the periphery due to vasodilation and stasis of blood flow

75
Q

process of forming granulation tissue in wound healing

A
  • fibroblast deposition of T3 collagen
  • capillary nutrient delivery
  • myofibirllast contraction of wound
76
Q

describe the relationship of arachidonic acid , COX, lipooxgenases, and TA2

A

phospholipid membranes have arachidonic acid which is cleaved/activated by phospholipase A2 to become either cyclooxgenases or lipooxgenases

COX

  • become Prostagladins (PGI2/E2/D2)
  • produce thromboxane A2 which causes vasoconstriction and platelet aggregating in primary hemostasis

LIPOX

  • become leukotrienes (LTB4, D4, E4, C4)
  • become LXA4/B4 which inhibit inflammation

**phospholipase A2 is inhibitd by steroids

77
Q

labile vs stable vs permanent tisses

A

labile = continuously dividing tissues capable of regeneration (ex: hemipoetic cells in bone marrow and surface epithelium )

stable= tissues normally in G0 stage but can proliferate in response to injury; limited regeneration ability (ex: liver, endothlial cells, fibroblasts, organ parenchyma, smooth M. cells)

permanent= tissues with no post-natal cell proliferation and no regeneration capacity (ex: heart , nerves, skeletal M.)

78
Q

what CTK recruits eosinophils

A

IL-5

79
Q

location of langerhans cells? alveolar Macrophages? histiocytes?

A
  1. skin
  2. lungs
  3. spleen and LNs
80
Q

what is a pro inflammatory protein made in the liver associated with DIC and activates coagulation and fibrinolytic systems with complement and Kinins

A

hageman factor

*activated with subendothelial exposure

81
Q

causes of exudate vs transudate

A

exudate (extracellular fluid high in protein and cell debris)
-caused by increased vascular permeability (as seen in acute inflammation)

transudate (extracellular fluid low in proteins)
-caused by change in osmotic equilibrium across capillary (increased hydrostatic pressure or decreased oncotic pressure)

82
Q

local/systemic signs in acute vs chronic inflammation

A

more prominent in acute inflammation (such as edema) vs chronic

83
Q

what is responsible for decreasing iron availability and causing anemia in chronic inflammation

A

hepcidin (iron regulator protein, increased in acute phase response )

84
Q

what are the two types of granulomatous inflammation and what are there hallmark differences

A

non-casseating
-no central necrosis

cosseting
-central necrosis

85
Q

what cell uses major basic protein and what is its function

A

eosinophils

-killls microbe by oxygen independent phagocytic killing

86
Q

healing by 1st intention vs 2nd intention of epithelial injury

A

1st intention **FIBROUS UNION
epithelial layer damage; tissue surfaces have been approximated; used when there has been very little tissue loss; leads to less scar formation

2nd intention

  • extensive injury, granulation tissue fills defect and results in more scarring and myofibrilblast attempt to decrease wound size
  • *WOUND CONTRACTION
87
Q

secretion of M1 MOs and function

A

IL-12 = induction of more IFN-Y
ROS , NO, and lysoszymes =l killing
IL-1/ TNF = fever and inflammation
IL-23 = more inflammation

88
Q

what are NETs function in acute inflammation

A

-fibrin nets made by neutrophils in response to pathogens that hold anti-microbial enzymes/granules near site of infection and are used as a net catch to trap the microbe for killing

89
Q

what is the source of PGs and LTs

A

mast cells and leukocytes

90
Q

morphologic features of chronic inflammation

A
  1. persistent infection/toxic exposure with extensive tissue destruction
  2. attempts of tissue repair by angiogenesis and fibrous
  3. mononuclear (macrophage, plasma cells, and lymphocytes) infiltration
91
Q

what are the 3 major components of acute inflammation and their consequences

A
  1. vasodilation
    - leads to increased blood flow through arteriole and to blood stasis at the post capillary venule
  2. increased vascular permeability
    - leads to exudative edema
  3. WBC emigration from blood and accumulation at injury followed by activation of elimination pathogenesis
92
Q

what is the normal amount of WBC in the body ? what is the amount seen in leukemiod reaction of luekyocytosis ?

A

4000-11000

40,000- 100,000

93
Q

IL-17 source and function

A

T-Cell (Th17)

  • nuetrophil recruitment
  • macrophage recruitment
  • *increases acute inflammation and chronic inflammation
  • *Th17 stimulated by IL-1
94
Q

what is needed for proper regeneration

A

ECM integrity
stem cells
growth factors for cell proliferation
**factors = intrinsic proliferative capacity

95
Q

source and function of platlet-activating factor (PAF)

A

leukocytes and mast cells

  • vasodilation
  • increased vascular permeability
  • leukyeocyte ahdesion
  • chemotaxis
  • degranulation
  • oxidative burst **!!!!!!!!!
96
Q

what does macrophages release that continues neutrophil recruitment and purulent inflammation

A

IL-8

Hannah MOD (6 decks)

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