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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
Q

contents of lysosomal granules released in ECM?

A
  • regurgitation = vacule open to outside

- frustrated phagocytosis =substances not easily ingested

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26
Q

LAD-1 vs LAD-2 defects in eukocyte adhesion

A

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)

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27
Q

chronic granulomatous disease

A

results from deficiency in a component of the phagocyte oxidase— no ROS

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28
Q

Chediak-Higashi Syndrome autosomal recessive disease

A
  • impaired fusion of lysosomes with phagosomes
  • secretion of lytic secretory granules by cytotoxic T-lymphocytes
  • severe immunodeficiency
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29
Q

resolution = _____ and _____ simutaneously

A

regeneration and repair

30
Q

fibrosis

A

extensive scarring inorgens

-occurs in organs where there is lots of CT; may compromise function (heart attack)

31
Q

what are the 3 morphological patterns of acute inflammation?

A

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
Q

blister vs bula

A 
blister= smaller than 1cm
bula= larger than 1cm
33
Q

think what when you hear purulent?

A

pus (cellulitis)

34
Q

ulcer vs erosion

A

ulcer= complete loss of epithilium, local, acute and chronic inflammation coexist

erosion= thining of epithium, larger earea

35
Q

cell derived mediators

A

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
Q

histamine

A
  • stored most commonly in mast cells (and basophiles and platelets)
  • released in response to injury, immune reactions, neuropeptides, cytokines
37
Q

serotonin

A

preformed mediators stored in platelets (also some in brain and GI)

  • causes vasoconstriction during clotting
  • released during platelet aggregation
38
Q

arachidonic acid metabolites

A
  • affect inflammation and hemostasis
  • WBCs, platelets, and mast cells are major sources
  • AA= component of cell membrane phospholipids
  • released by action of phospholipases
39
Q

COX1 vs COX2 inhibitors

A

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
Q

aspirin and NSAID inhibit ________ and treat?

A

inhibit cyclooxygenase (COX 1 and 2)

  • block PG synthesis
  • treat pain and fever
41
Q

glucocorticoids inhibit what part of arachidonic acid (AA) pathway?

A

inhibits phospholipases A2–> inhibits AA release and production of prostaglandins and leukotrienes bc it is at the TOP of the pathway

42
Q

what are cytokines?

role in acute and chronic inflammation?

A

mediators of inflammation and immune response

  • acute inflammation = tumor necrosis factor (TNF), IL 1 and 6
  • chronic = interferon- gamma and IL-12
43
Q

IL-17 produced by?

A

T-cell mostly

44
Q

TNF and IL-1 primary role?

A

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
Q

cachexia

A

metabolic wasting with chronic illness

46
Q

RANTES

A

regulates on activation, Normal T-cell Expressed and Secreted
*chemotactic for memory CD4+ T-cells and monocytes

47
Q

eotaxin

A

chemotactic for eosinophils

48
Q

ROS released from? stored in?

A
  • released from neutrophils and macrophages
  • within lysosomes
  • short lived
  • stored in liver
49
Q

nitric oxide

A

short-lived, soluble, free radical

  • in CNS regulates neurtransmitter release and blood flow
  • produced by endothelial cells
  • antagonizes platelet activation
50
Q

what are the lysosomal enzymes of leukocytes?

A

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
Q

substance P

A

is a neuropeptide

  • transmits pain signals
  • regulation of vessel tone
  • modulate vascular permeability
52
Q

what do complement proteins do upon activation?

A
  • opsonize microbes to facilitate phagocytosis
  • increase vascular permeability
  • generation of membrane attack complex
53
Q

inactive components of complement?

A

C1-C9

54
Q

complement is activated how?

A

proteolysis leading to a cascade

55
Q

activation of C3

A

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
Q

What makes up C5 convertase?

A

C3b binding to C3 convertase complex

57
Q

C3b is deposited on surface of?

A

a microbe

58
Q

C5 convertase–>

A

C5a and C5b –> assembly of C6-C9

59
Q

MAC’s composition =

A

C5b- C6- C7- C8-C9n

60
Q

C3a and C5a are both?

A

anaphylatoxins: mast cells release histamine and increase vascular permeability

61
Q

C5a acitves ______ pathway of AA metabolism

A

lipoxygenase

62
Q

decay accelerating factor

A

limits formation of C3 and C5 convertase. acquired deficiency of DAF–> paroxysmal nocturnal hemoglobinuria

63
Q

Factor H

A

also limits convertase formation.

64
Q

Hagemen factor or factor 12 (active form 12a) activates?

A
  • kinin system
  • clotting system
  • fibrinolytic system
  • complement system
65
Q

Hagemen factor is synthesized where? activated when in contact with?

A
  • synthesized in liver

- active when contacting collagen

66
Q

factor 12a > ______ (factor 2) and _____ (factor 2a) > cleavage of ______ > _____ clot

A

factor 12a > prothrombin (factor 2) and thrombin (factor 2a) > cleavage of fibrinogen > fibrin clot

67
Q

factor 10a

A

increase vascular permeability and WBC adhesion

68
Q

factor 12a ultimately leads to?

A

bradykinin, which causes pain and has similar affects as histamine

69
Q

bradykinin

A 
causes paiin
-similar affects as histamine
0increase vascular perm
-arteriolar dilation
-bronchial smooth muscle contraction
70
Q

kallikrain has chemotactic activitiy and activates?

A

Hagement (12a) factor like a feed back loop

Pathology 1 (21 decks)

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