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PB+T > Inflammation Path > Flashcards

Inflammation Path Flashcards

0
Q

Acute vs chronic inflammation

A

Acute: neutrophils + edema
- seconds initiation days duration
Chronic: macrophages/ lymphocytes + repair

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1
Q

Inflammation

A

Vascular response to injury/stress leading to the accumulation of protein rich fluid and activate leukocytes to tissue

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2
Q

Three components of acute inflammation

A

Vasodilation (seconds)
Increased permeability (minutes)
Migration of neutrophils (minutes - hours)

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3
Q

Ex/trans/purulent exudate

A

Transudate: mostly water, oncotic shift (HTN, starvation) low specific gravity (< 1.020)
Exudate: water, protein, cell debris (s.g. > 1.020)
Purulent exudate: exudate with neutrophils and apoptotic debris

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4
Q

Mechanisms of increased vascular permeability

A
  • Gaps in venules due to endothelial contraction
  • Endothelial injury (punching holes)
  • Leukocyte adhesion and damage of endothelium in venules and capillaries
  • transcytosis via interconnected vesicles and vacuoles (VEGF mediated)
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5
Q

Extravisation of leukocytes

A

Adhesion via P-selectins stored in weible pilade bodies (released by histamine and thrombin, and synthesized because of the signal IL-1 and TNF signal from macs) in endothelium binding sialyated gptns, and ICAMs on endothelium binding integrins (CD54). Chemokines released from tissue at sight of injury bind leukocytes and increase integrin avidity. Increase permeability allows diapedesis through capillary wall.

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6
Q

Chemotaxis: endogenous, exogenous

A

Exogenous: bacterial products
Endogenous: C5a, LTB4, cytokines (IL5-eosinophils, IL8-eosinophils and basophils, IL17 - attracts monocytes/neutrophils)

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7
Q

CD14

A

LPS receptor

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8
Q

CD31

A

Platelet adhesion molecules

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9
Q

CD44

A

Leukocyte to ECM binding

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10
Q

CD54

A

Integrin

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11
Q

IL1-5

A 
1-Hot
2-T-cell proliferation 
3-Bone marrow stimulation 
st
4-E (IgE)
5-A (IgA) 
k
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12
Q

3 steps in phagocytosis

A

Attachment: receptor binding
Engulfment: phagosome IP3/DAG
Destruction: phagolysosomes (MPO HOCl OH OONO)

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13
Q

Oxygen independent killing

A

Lysozyme, MBP, acid hydrolase

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14
Q

LAD 1/2

A

1 beta chain of integrin sect

2 lack of Sialyated oligosaccarides (no fucosyl transferase)

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15
Q

XLCGD/CGD

A

XL: membrane component of oxidative burst missing (NADPH oxidase defective)

Normal: cytoplasmic Ox burst missing (NADPH oxidase defective)

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16
Q

MPO deficiency

A

MPO- H2O2 halide killing defective

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17
Q

Chediak-Higasi syndrome

A

Defective microbial liking due to ineffective lysosomal docking/fusing

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18
Q

Leukopenia

A

Bone marrow suppression

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19
Q

Acquired Adhesion/chemotaxis defect

A

DM, cancer, sepsis, chronic dialysis

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20
Q

Acquired defective phagocytosis and microbiocidal activity

A

Leukemia, anemia, sepsis, DM, malnutrition premature neonates

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21
Q

Chemical mediators of inflammation

A

Histamine, serotonin, lysozymal act, eicosenoid derivatives, factor XII -> kinins, clotting factors and compliment

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22
Q

Azeurophilic granules/specific granules

A

Azeuophilic: Contain myeloperoxidase
Specific: lactoferrin

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23
Q

Sources of histamine: 3

A

Basophils, mast cells, platelets

- vasoactive amine H1 release, H2 negative feedback reduce.

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24
Q

Compliment components

A

C3a, C5a anaphalaxins
C5a is strongly chemotactic for neutrophils
C3b fixes compliment
C5b MAC

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25
Q

Thrombin in inflammation

A

Binds PAR-1 which is proinflammatory

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26
Q

NO in inflammation

A

Paracrine: seconds duration
Results in vasodilation -> contributes to margination
iNOS also contributes to microbiocidal activity producing peroxynitrite (OONO)

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27
Q

A.C.E.

A

Vitamins A, C and E reduce free radicals

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28
Q 
Vasodilation
Vascular permeability
Chemotaxis
Fever
Pain
Tissue damage
A

NO, histamine, PGE
Histamine, serotonin, C3,C5a, Bradykinin, PAF
TNF, ILs,

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29
Q

IL-12

A

Secreted by MACS; convert naive CD4 T cells into active TH1 cells.
- happens in process to granuloma formation

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30
Q

Granulomatous inflammation

A

Caseating; TB, fungus, syphillis
- langhans cells, central area of necrosis
Non-caseating; mycobacterium, sarcoidosis, many other infections

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31
Q

Serous inflammation

A

Bullous, watery filled vesicles with few inflammatory cells

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32
Q

Fiberous inflammation

A

Shaggy, occurs when larger proteins escape the vessels (HTN, oncotic shift) “bread and butter”

33
Q

Supperative inflammation

A

Purulent: neutrophils, fiberous necrotic cell debris usually filling abscess

34
Q

Fever

A

IL-1, TNF chrom MACs .stimulate conversion of AA into PGEs. PGE2 facilitates temp increase.
Involves endocrine and CNS
- CRP non-specific for cause or type of inflammation, but highly sensitive for inflammation itself

35
Q

Defensins and cathelicidens

A

Cationic arginine rich granule peptides (defensins) that are microbiocidal and Found in neutrophils (both)

36
Q

Lysozyme: function

A

Hydrolyzes the muramic acid - N Acetylglucosamine bond in GPTNS of bacterial coats

37
Q

Lactoferrin

A

Binds iron so that bacteria can’t get it. It’s an essential metabolite for many microbes.

38
Q

Major Basic Protein

A

Anti paracytic protein with limited bacteriocidal capacity

39
Q

Classic vs alternative activation of macs

A

Classic: TLR/INFg. Results in killer macs responsible for bacteriocidal activity (ROS,NO) and pathological inflammation (IL-1,IL-12 and IL-23)

Alternate: IL-4, 13-13. Results in regulators of inflammation (IL-10, TGFB) and wound healing (arginase, proline, polyaminases, TGFB)

40
Q

CGD: XL and recessive (Robbins info)

A

XL: males only, PM component of the phagocyte oxidase (gp91phox)
Reces: cytoplasmic component of phag. ox. (gp47phox, gp67phox)

41
Q

Lipoxin A4/B4: function and production

A

Anti-inflammatory agents: Inhibit neutrophil adhesion and chemotaxis. LTB4 action is antagonistic
Has CTL cytotoxicity
- AA - 5-LOX-> 5-HPETE -> 12-LOX-> lipoxin

42
Q

Cellular Effect from Release of ROS: 2 (one general, one specific)

A

Endothelial tissue damage (endothelial cells and parenchyma et al) and inactivation of antiproteases like a1antitrypsin

43
Q

5 ROS mediators

A

Glutathione system, catalase, superoxide dismutase, ceruloplasmin, transferrin

44
Q

NO: function and synthesis

A

Synthesized by NOS (endothelial, neuronal and inducible forms) from L-Arginine
Vasodilation (vasc. Sm. muscle relaxation), inhibition of cellular inflammatory response. (Reduced leukocyte adhesion)
- NO and it’s derivatives are bacteriocidal

45
Q

Three mechanisms of activating mast cells

A

Tissue trauma
C3a/C5a
Cross linking IgE

46
Q

Regulators of integrins and selectins

A

Selectins: P-selectins (from Weible Pilade bodies) regulate by histamine; E selectins are induced via TNF and IL-1

Integrins: C5a, LTB4

47
Q

IL-8

A

Neutrophils called in by MACS via IL-8

48
Q

Causes of Granuloma formation

A

Tb, fungi (caseating)

Sarcoidosis, cat scratch and brucellosis, syphillis some mycoses

49
Q

Alpha chemokines

A

CXC- primarily act on neutrophils (mainly IL-8) secreted by activated macs

50
Q

Beta chemokines

A

C-C: MCP/MIP/RANTES

- act on/attract monocytes, eosinophils, basophils

51
Q

Gamma chemokines

A

C- lymphotactin

52
Q

CXC3

A

fractalkine: monocyte/lymphocyte adhesion

53
Q

Three effects of compliment

A

Inflammation - C3/5a
Phagocytosis - C3b
Lysis - C5b

54
Q

Hageman factor

A

Factor 12 cross point of inflammation (accessing the kinin pathway) and clotting (thrombin plasmin et al)
- both plasmin and killikrein feedback and can activate factor 12

55
Q

Foreign body granuloma

A

Contains giant cells that are haphazard organized

56
Q

Acute phase proteins: 3

A

Respond immediately to acute inflammation, result in an increased sed rate
CRP, fibrinogen - induced from IL-6
Serum amyloid A - IL-1, TNF
- CRP, SAA: help fix compliment

57
Q

Non-specific markers for inflammation

A
  • Increased sed rate: resultant from fibrinogen release (acute phase response)
  • increased CRP
58
Q

Fractalkine

A

CXC - lymphocyte/monocyte adhesion

59
Q

Ceruloplasmin

A

Copper binding ROS mediator

60
Q

Activation of hageman factor (XII)

A

Contact with negatively charged surfaces (cell under stress)

61
Q

SAAIL1

A

Serum amyloid A IL1/TNF

62
Q

Hot T Bone stEAk Cooked in Fat

A 
IL-1 Hot (fever) 
IL-2 T (t cell proliferation) 
IL-3 B (b cell activation) 
IL-4 E (IgG - IgE conversion) 
IL-5 A (IgG - IgA conversion, eosinophils) 
IL-6 Crp, Fibrin
63
Q

1,12,23

A

ILs produced in classical compliment path activation

64
Q

Fat necrosis

A

Pancreatic injury - tissue surrounding the pancreas; the pancreas parenchyma undergoes liquifactive necrosis.

65
Q

Breastfeeding cellular change

A

Lobular hypertrophy/hyperplasia

66
Q

Atalectaisis

A

Collapsed alvioli

67
Q

Metaproterenol

A

Only B2 agonist that is IM

iM-Meta

68
Q

IL-1(2)

A

Fever and selectin expression.

69
Q

IL-8

A

Secreted by all cells with TLRs: Neutrophils and basophils attractant
(Noodles and it looks like a B)

70
Q

IL-10

A

Immunosuppressive, thelpers, tregs

71
Q

IL-12

A

Primary TH1 activator. Loops with IFNg to control microbial infection.
12 conTrols Tcell

72
Q

IL-17

A

Neutrophil AND monocyte chemotactic. It’s chronic.(17 y/os are chronic offenders)

73
Q

gp91

gp47,67

A
  • plasma membrane protein mutation in XL CGD

- cytoplasmic proteins mutated in CGD

74
Q

FLIP

A

Anti-apoptotic

- viruses secrete to keep the cell from killing itself

75
Q

Certulin

A

Increase life span

- red wine (grapes) being skinny

76
Q

Plasmin in neutrophil recruitment

A

Directly cleave C3a -> anaphylaxin

77
Q

Two common forms of metaplasia

A

Squamous -> columnar: esophageal epi accommodates mucus secreting cells (gastric reflux)

Columnar -> squamous: bronchial epi changes to accommodate smoke; tougher, but can’t move mucus.

78
Q

Wet v.dry necrosis

A

Imposed superinfection (wet) no superinfection (dry)

79
Q

Bcl

A

First IDd in B cell Lymphoma (BcL)

- anti apoptotic sensor protein: senses DNA damage and lack of signal

80
Q

Eotaxin

A

Eosinophil chemotactic factor

81
Q

Alcoholic induced cirrhosis

A

Cellular changes include build up of keratin filaments in the cells

PB+T (20 decks)

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