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
Compliment components
C3a, C5a anaphalaxins C5a is strongly chemotactic for neutrophils C3b fixes compliment C5b MAC
25
Thrombin in inflammation
Binds PAR-1 which is proinflammatory
26
NO in inflammation
Paracrine: seconds duration Results in vasodilation -> contributes to margination iNOS also contributes to microbiocidal activity producing peroxynitrite (OONO)
27
A.C.E.
Vitamins A, C and E reduce free radicals
28
``` Vasodilation Vascular permeability Chemotaxis Fever Pain Tissue damage ```
NO, histamine, PGE Histamine, serotonin, C3,C5a, Bradykinin, PAF TNF, ILs,
29
IL-12
Secreted by MACS; convert naive CD4 T cells into active TH1 cells. - happens in process to granuloma formation
30
Granulomatous inflammation
Caseating; TB, fungus, syphillis - langhans cells, central area of necrosis Non-caseating; mycobacterium, sarcoidosis, many other infections
31
Serous inflammation
Bullous, watery filled vesicles with few inflammatory cells
32
Fiberous inflammation
Shaggy, occurs when larger proteins escape the vessels (HTN, oncotic shift) "bread and butter"
33
Supperative inflammation
Purulent: neutrophils, fiberous necrotic cell debris usually filling abscess
34
Fever
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
Defensins and cathelicidens
Cationic arginine rich granule peptides (defensins) that are microbiocidal and Found in neutrophils (both)
36
Lysozyme: function
Hydrolyzes the muramic acid - N Acetylglucosamine bond in GPTNS of bacterial coats
37
Lactoferrin
Binds iron so that bacteria can't get it. It's an essential metabolite for many microbes.
38
Major Basic Protein
Anti paracytic protein with limited bacteriocidal capacity
39
Classic vs alternative activation of macs
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
CGD: XL and recessive (Robbins info)
XL: males only, PM component of the phagocyte oxidase (gp91phox) Reces: cytoplasmic component of phag. ox. (gp47phox, gp67phox)
41
Lipoxin A4/B4: function and production
Anti-inflammatory agents: Inhibit neutrophil adhesion and chemotaxis. LTB4 action is antagonistic Has CTL cytotoxicity - AA - 5-LOX-> 5-HPETE -> 12-LOX-> lipoxin
42
Cellular Effect from Release of ROS: 2 (one general, one specific)
Endothelial tissue damage (endothelial cells and parenchyma et al) and inactivation of antiproteases like a1antitrypsin
43
5 ROS mediators
Glutathione system, catalase, superoxide dismutase, ceruloplasmin, transferrin
44
NO: function and synthesis
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
Three mechanisms of activating mast cells
Tissue trauma C3a/C5a Cross linking IgE
46
Regulators of integrins and selectins
Selectins: P-selectins (from Weible Pilade bodies) regulate by histamine; E selectins are induced via TNF and IL-1 Integrins: C5a, LTB4
47
IL-8
Neutrophils called in by MACS via IL-8
48
Causes of Granuloma formation
Tb, fungi (caseating) | Sarcoidosis, cat scratch and brucellosis, syphillis some mycoses
49
Alpha chemokines
CXC- primarily act on neutrophils (mainly IL-8) secreted by activated macs
50
Beta chemokines
C-C: MCP/MIP/RANTES | - act on/attract monocytes, eosinophils, basophils
51
Gamma chemokines
C- lymphotactin
52
CXC3
fractalkine: monocyte/lymphocyte adhesion
53
Three effects of compliment
Inflammation - C3/5a Phagocytosis - C3b Lysis - C5b
54
Hageman factor
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
Foreign body granuloma
Contains giant cells that are haphazard organized
56
Acute phase proteins: 3
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
Non-specific markers for inflammation
- Increased sed rate: resultant from fibrinogen release (acute phase response) - increased CRP
58
Fractalkine
CXC - lymphocyte/monocyte adhesion
59
Ceruloplasmin
Copper binding ROS mediator
60
Activation of hageman factor (XII)
Contact with negatively charged surfaces (cell under stress)
61
SAAIL1
Serum amyloid A IL1/TNF
62
Hot T Bone stEAk Cooked in Fat
``` 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
1,12,23
ILs produced in classical compliment path activation
64
Fat necrosis
Pancreatic injury - tissue surrounding the pancreas; the pancreas parenchyma undergoes liquifactive necrosis.
65
Breastfeeding cellular change
Lobular hypertrophy/hyperplasia
66
Atalectaisis
Collapsed alvioli
67
Metaproterenol
Only B2 agonist that is IM | iM-Meta
68
IL-1(2)
Fever and selectin expression.
69
IL-8
Secreted by all cells with TLRs: Neutrophils and basophils attractant (Noodles and it looks like a B)
70
IL-10
Immunosuppressive, thelpers, tregs
71
IL-12
Primary TH1 activator. Loops with IFNg to control microbial infection. 12 conTrols Tcell
72
IL-17
Neutrophil AND monocyte chemotactic. It's chronic.(17 y/os are chronic offenders)
73
gp91 | gp47,67
- plasma membrane protein mutation in XL CGD | - cytoplasmic proteins mutated in CGD
74
FLIP
Anti-apoptotic | - viruses secrete to keep the cell from killing itself
75
Certulin
Increase life span | - red wine (grapes) being skinny
76
Plasmin in neutrophil recruitment
Directly cleave C3a -> anaphylaxin
77
Two common forms of metaplasia
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
Wet v.dry necrosis
Imposed superinfection (wet) no superinfection (dry)
79
Bcl
First IDd in B cell Lymphoma (BcL) | - anti apoptotic sensor protein: senses DNA damage and lack of signal
80
Eotaxin
Eosinophil chemotactic factor
81
Alcoholic induced cirrhosis
Cellular changes include build up of keratin filaments in the cells