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Pathology 1 > Inflammation repair > Flashcards

Inflammation repair Flashcards

1
Q

acute inflammation

A
  • rapid onset
  • short duration (few minutes to days)
  • fluid and plasma protein exudation
  • predominantly neutrophilic leukocyte accumulation
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2
Q

chronic inflammation

A
  • more insidious
  • longer duration (days to years)
  • influx of lymphocytes and macrophages
  • vascular proliferation and fibrosis (scarring)
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3
Q

circulating inflammatory cells

A 
neutrophils
lymphocytes
monocytes
eosinophils
basophils
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4
Q

extravascular inflammatory cells

A

macrophages
mast cells
dendritic cells

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5
Q

cardinal signs of inflammation?

A 
heat
redness
swelling 
pain
loss of funcion
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6
Q 
calor=
rubor= 
tumor= 
dolor=
functio laesa=
A 
heat
redness
swelling 
pain
loss of funcion
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7
Q

transudate

A
  • ultrafiltrate of blood plasma
  • low protein conent
  • results from hydrostatic alterations across the vascular endothelium
  • permeability of the endothelium is normal
  • may accumulate in various non-inflammatory conditions
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8
Q

exudate

A
  • protein rich fluid and cellular debris
  • result of increased vascular permeability
  • typical of inflammation
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9
Q

mechanisms of increased vascular permeability

A

1) endotheliall cell retraction
- -immediate Transient response
- -caused by chemical mediators (histamine, bradykinin, leukotrienes)
2) endothelial injury
- -immediate sustained response
3) increased transcytosis
- -mediated by vascular-endothelial growth factor (VEGF)
4) leakage from new blood vessels
- -angiogenesis during wound healing

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10
Q

BV + fibroblasts= _____ tissue

A

granulation tissue

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11
Q

leukocyte recruitment

A
  • margination
  • rolling (SELECTIN family of adhesion molecules)
  • adhesion (integrins on leukocytes)
  • transmigration (chmokines and CD31)
  • chemotaxis
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12
Q

leukocyte activation

A
  • phagocytosis

- killing and degradation of microbes

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13
Q

another term for transmigration?

A

diapedesis

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14
Q

complement component C5a and lipoxygenase pathway of AA metabolism (LTB) are ______ agents

A

chemotaxic

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15
Q

when does neutrophils predominate over monocytes in inflammation response? which one survives longer?

A

neutrophils predominate in first 24 hours!

**monocytes survive longer

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16
Q

3 steps of phagocytosis

A

1) recognition and attachment
2) engulfment and formation of phagocytic vacuole
3) killing and degradation

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17
Q

what do opsonins do?

A

host proteins that coat microbes and target them for phagocytosis (by a process called opsonization)

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18
Q

important opsonins

A
  • IgG antibodies
  • breakdown products of complement protein C3
  • collectins
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19
Q

leukocyte receptors

A
  • Fc receptor for IgG
  • complement receptors (CR 1 and 3)
  • C1q receptors for collectins
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20
Q

myeloperoxidase

A

an enzyme contained in neutrophile lysosomes

*converts H2O2 to HOCl (powerful antimicrobial agant and oxidant)

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21
Q

dead microorganisms are degraded by _______

A

lysosomal acid hydrolases (elastase)

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22
Q

besides lysosomal acid hydrolases, what are other antimicrobials in leukocyte granules?

A
  • bactericidal permeability-increasing protein
  • lysozyme
  • major basci protein
  • defensins (create holes in membranes)
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23
Q

phagocytic mechanisms are primarily confined to ________. but what about leukocytes?

A

phagolysosome

* but leukocytes may secrete enzymes and antimicrobial peptides into the extracellular space

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24
Q

neutrophil extracellular traps

A
  • nuclear chromatin + granule protein
  • detected in blood neutrophils during sepsis
  • fibrilar networks produced in response to infectious pathogens
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25
contents of lysosomal granules released in ECM?
- regurgitation = vacule open to outside | - frustrated phagocytosis =substances not easily ingested
26
LAD-1 vs LAD-2 defects in eukocyte adhesion
LAD-1 =defective syntehsis of CD18 B subunit of LFA-1 and Mac-1= IMPAIRED ADHESION LAD-2 =defect in fucose metabolism- absence of sialyl-Lewis X (polysac surface of WBCs)
27
chronic granulomatous disease
results from deficiency in a component of the phagocyte oxidase--- no ROS
28
Chediak-Higashi Syndrome autosomal recessive disease
- impaired fusion of lysosomes with phagosomes - secretion of lytic secretory granules by cytotoxic T-lymphocytes - severe immunodeficiency
29
resolution = _____ and _____ simutaneously
regeneration and repair
30
fibrosis
extensive scarring inorgens | -occurs in organs where there is lots of CT; may compromise function (heart attack)
31
what are the 3 morphological patterns of acute inflammation?
1) serous - -watery, protein poor, mesothelial cells lining the cavities 2) fibrous - -more serious, pink mesh looking, fibrin removed by macrophages (resolution) 3) suppurative (purulent) - -PUS, strep and staph, cellulitis
32
blister vs bula
``` blister= smaller than 1cm bula= larger than 1cm ```
33
think what when you hear purulent?
pus (cellulitis)
34
ulcer vs erosion
ulcer= complete loss of epithilium, local, acute and chronic inflammation coexist erosion= thining of epithium, larger earea
35
cell derived mediators
1) vasoactive amines - -histamine and serotonin 2) arachidonic acid metabolites - - prostaglandins, leukotrienes, lipoxins 3) platelet-activating factor 4) cytokines - - tumor necrosis factor, interleukin-1, chemokines 5) ROS 6) nitric oxide 7) lysosomal enzymes of leukocytes 8) neuropeptides
36
histamine
- stored most commonly in mast cells (and basophiles and platelets) - released in response to injury, immune reactions, neuropeptides, cytokines
37
serotonin
preformed mediators stored in platelets (also some in brain and GI) - causes vasoconstriction during clotting - released during platelet aggregation
38
arachidonic acid metabolites
- affect inflammation and hemostasis - WBCs, platelets, and mast cells are major sources - AA= component of cell membrane phospholipids - released by action of phospholipases
39
COX1 vs COX2 inhibitors
COX1= inhibition of COX1 is bad bc is protects stomach against acid COX2= is better to block bc it is not produced in normatl tissues
40
aspirin and NSAID inhibit ________ and treat?
inhibit cyclooxygenase (COX 1 and 2) - block PG synthesis - treat pain and fever
41
glucocorticoids inhibit what part of arachidonic acid (AA) pathway?
inhibits phospholipases A2--> inhibits AA release and production of prostaglandins and leukotrienes bc it is at the TOP of the pathway
42
what are cytokines? | role in acute and chronic inflammation?
mediators of inflammation and immune response * acute inflammation = tumor necrosis factor (TNF), IL 1 and 6 * chronic = interferon- gamma and IL-12
43
IL-17 produced by?
T-cell mostly
44
TNF and IL-1 primary role?
endothelial activation and may enter circulation to induce systemic acute phase reaction (cachexia, lethargy) * TNF= inrease thromogenicity and neutrophil aggregation * IL-1 = fibroblast activation
45
cachexia
metabolic wasting with chronic illness
46
RANTES
regulates on activation, Normal T-cell Expressed and Secreted *chemotactic for memory CD4+ T-cells and monocytes
47
eotaxin
chemotactic for eosinophils
48
ROS released from? stored in?
- released from neutrophils and macrophages - within lysosomes - short lived - stored in liver
49
nitric oxide
short-lived, soluble, free radical - in CNS regulates neurtransmitter release and blood flow - produced by endothelial cells - antagonizes platelet activation
50
what are the lysosomal enzymes of leukocytes?
1) acid proteases - active within phagolysosomes 2) neutral protease - -cleaves C3 and C5 to C3a and C5a 3) counteracted by antiproteases - -alpha 1-antitrypsin (inhibits neutrophil elastase) - -alpha 2- macrophages
51
substance P
is a neuropeptide - transmits pain signals - regulation of vessel tone - modulate vascular permeability
52
what do complement proteins do upon activation?
* opsonize microbes to facilitate phagocytosis * increase vascular permeability * generation of membrane attack complex
53
inactive components of complement?
C1-C9
54
complement is activated how?
proteolysis leading to a cascade
55
activation of C3
C3 convertase --> C3a and C3b 1) classical pathway triggered by binding of C1 to Ag-Ab complexes 2) alternative pathway triggered by endotoxin, other cell wall components 3) lectin pathway: binding of plasma lectin to mannose residues on microbes
56
What makes up C5 convertase?
C3b binding to C3 convertase complex
57
C3b is deposited on surface of?
a microbe
58
C5 convertase-->
C5a and C5b --> assembly of C6-C9
59
MAC's composition =
C5b- C6- C7- C8-C9n
60
C3a and C5a are both?
anaphylatoxins: mast cells release histamine and increase vascular permeability
61
C5a acitves ______ pathway of AA metabolism
lipoxygenase
62
decay accelerating factor
limits formation of C3 and C5 convertase. acquired deficiency of DAF--> paroxysmal nocturnal hemoglobinuria
63
Factor H
also limits convertase formation.
64
Hagemen factor or factor 12 (active form 12a) activates?
- kinin system - clotting system - fibrinolytic system - complement system
65
Hagemen factor is synthesized where? activated when in contact with?
- synthesized in liver | - active when contacting collagen
66
factor 12a > ______ (factor 2) and _____ (factor 2a) > cleavage of ______ > _____ clot
factor 12a > prothrombin (factor 2) and thrombin (factor 2a) > cleavage of fibrinogen > fibrin clot
67
factor 10a
increase vascular permeability and WBC adhesion
68
factor 12a ultimately leads to?
bradykinin, which causes pain and has similar affects as histamine
69
bradykinin
``` causes paiin -similar affects as histamine 0increase vascular perm -arteriolar dilation -bronchial smooth muscle contraction ```
70
kallikrain has chemotactic activitiy and activates?
Hagement (12a) factor like a feed back loop

Pathology 1 (21 decks)

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