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==Pathophysiology of ILD==
==Pathophysiology of ILD==
{{Family tree/start}}
{{Family tree/start}}
{{Family tree| | | | | | | | | | | | | | | | | | | | | T01 | | | | | | | | | | | | | | | T01=Tissue injury}}
{{Family tree| | | | | | | | | | | | | | | | | | | | | | | T01 | | | | | | | | | | | | T01=Tissue injury in lungs}}
{{Family tree| | | | | | | | | | | | | |,|-|-|-|-|-|-|-|^|-|-|-|-|-|-|-|.| | | | | | | | }}
{{Family tree| | | | | | | | | | | | | | | | | |,|-|-|-|-|-|^|-|-|-|-|-|.| | | | | | | | }}
{{Family tree| | | | | | | | | | | | | S01 | | | | | | | | | | | | | | S02 | | | | | | | S01=Epitehelial injury|S02=Vascular injury}}
{{Family tree| | | | | | | | | | | | | | | | | S01 | | | | | | | | | | S02 | | | | | | | S01=Epitehelial injury|S02=Vascular injury}}
{{Family tree| | | | | | | | | | | | | |!| | | | | | | | | | | | | | | |!| | | | | | | | }}
{{Family tree| | | | | | | | | | | | | | | | | |!| | | | | | | | | | | |!| | | | | | | | }}
{{Family tree| | | | | | R01 | | | | | |!| | | | | | R01 | | | | | | | R02 | | | | | | | R01=Mast cells|R02= LPA6, LPA2, and LPA4 receptors }}
{{Family tree| | | | | | | | R01 | | | | | | | |!| | | | | | | | | | | R02 | | | | | | | R01=Mast cells in lungs|R02= LPA6, LPA2, and LPA4 receptors }}
{{Family tree| | | | | | |!| | | | | | |!| | | | | | |!| | | | | | |,|-|^|-|.| | | | | | }}
{{Family tree| | | | | | |,|-|^|-|.| | | | | | |!| | | | | | | | | |,|-|^|-|.| | | | | | }}
{{Family tree| | Q01 | | |!| | | | | | Q02 | | | | | Q03 | | | | | Q04 | | Q05 | | | | | Q01=Decreased sFRP-1 (secreted frizzled-related protein 1) in fibroblasts|Q02= Insulin-like growth factor (IGF) signalling|Q03=Transforming growth factor (TGF)-β|Q04= Reduced expression of angiogenic factors,<br>vascular endothelial growth factor (VEGF)|Q05=Elevation of angiostatic factors,<br>pigment epithelium-derived factor}}
{{Family tree| | Q01 | | Q06 | | Q03 | | | | | Q02 | | | | | | | | Q04 | | Q05 | | | | | Q01=Decreased sFRP-1 (secreted frizzled-related protein 1) in fibroblasts|Q02= Insulin-like growth factor (IGF) signalling|Q03=Transforming growth factor (TGF)-β|Q04= Reduced expression of angiogenic factors,<br>vascular endothelial growth factor (VEGF)|Q05=Elevation of angiostatic factors,<br>pigment epithelium-derived factor|Q06=Secretes tryptase}}
{{Family tree| | |!| | | |!| | | |,|-|-|^|-|-|.| | | |!| | | | | | |`|-|v|-|'| | | | | | }}
{{Family tree| | |!| | | |!| | | |!| | | |,|-|-|^|-|-|.| | | | | | |`|-|v|-|'| | | | | | }}
{{Family tree| | P01 | | P02 | | P03 | | | | P04 | | P05 | | | | | | | P06 | | | | | | | P01=Wnt/β-catenin signalling pathway|P02=Tryptase|P03=IGF-binding protein 3 (IGFBP-3)|P04=IGF-binding protein 5 (IGFBP-5)|P05=Upregulation of Egr-1 (early growth response protein 1)|P06=Loss of endothelial barrier function }}
{{Family tree| | P01 | | P02 | | P05 | | P04 | | | | P03 |.| | | | | | | | P06 | | | | | P01=Wnt/β-catenin signalling pathway|P02=PAR-2/protein kinase (PK)C-α/Raf-1/p44/42 signaling pathway|P03=IGF-binding protein 3 (IGFBP-3)|P04=IGF-binding protein 5 (IGFBP-5)|P05=Upregulation of Egr-1 (early growth response protein 1)|P06=Loss of endothelial barrier function }}
{{Family tree| |!| |!| | |!| | |!| |!| | | | |`|-|v|-|'| | | | | | | | |!| | | | | | | | }}
{{Family tree| |!| |!| | |!| | | |!| | | |!| | | | | |!| |!| | | | | | |!| | | | | | | | }}
{{Family tree| O01 |!| | |!| O02 | |!| | | | | | |!| | | | | | | | | | |!| | | | | | | | O01=Dysregulation of repair|O02=Regulates transforming growth factor (TGF)-β }}
{{Family tree| O01 |!| | |!| | | |`|-|-|-|^|.| | | | |!| O02 | | | | | |!| | | | | | | | O01=Dysregulation of repair in lung tissue|O02=Regulates transforming growth factor (TGF)-β }}
{{Family tree| | | |!| | |!| | |`|.|!| | | | | | |!| | | | | | | | | | |!| | | | | | | | }}
{{Family tree| | | |!| | |!| | | | | | | | |!| | | | |!|,|'| | | | | | |!| | | | | | | | }}
{{Family tree| | | |!| | A01 | | | A02 | | | | | |!| | | | | | | | | | |!| | | | | | | | A01=PAR-2/protein kinase (PK)C-α/Raf-1/p44/42|A02=Induction of syndecan-2 (SDC2)}}
{{Family tree| | | |!| | |!| | | | | | | | |!| | | | A02 | | | | | | | |!| | | | | | | | A01=|A02=Induction of syndecan-2 (SDC2)}}
{{Family tree| | | |!| | |!| | | | |`|-|-|-|.| | |!| | | | | | | | | | |!| | | | | | | | }}
{{Family tree| | | |!| | |!| | | | | | | | |!| | | | |!| | | | | | | | |!| | | | | | | | }}
{{Family tree| | | |!| | |`|-|-|-|-|-|-|-|.|!|,|-|'| | | | | | | | | | |!| | | | | | | | }}
{{Family tree| | | |!| | |`|-|-|-|-|-|-|-|.|!|,|-|-|-|'| | | | | | | | |!| | | | | | | | }}
{{Family tree| | | |`|-|-|-|-|-|-|-|-|-|-| B01 | | | | | | | | | | | | |!| | | | | | | | B01=Activation,proliferation, and migration of fibroblast to the site of injury}}
{{Family tree| | | |`|-|-|-|-|-|-|-|-|-|-| B01 | | | | | | | | | | | | |!| | | | | | | | B01=Activation,proliferation, and migration of fibroblast to the site of injury}}
{{Family tree| | | | | | | | | | | | | | | |!| | | | | | | | | | | | | |!| | | | | | | | }}
{{Family tree| | | | | | | | | | | | | | | |!| | | | | | | | | | | | | |!| | | | | | | | }}
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{{Family tree| | | | | | | | | | | | | | | |!| | | |!| J02 | | | J03 | |!| | | | | | | | J02=Different ranges of contractions mediated by RhoA/Rho-associated kinase|J03=Changes in intracellular calcium concentrations}}
{{Family tree| | | | | | | | | | | | | | | |!| | | |!| J02 | | | J03 | |!| | | | | | | | J02=Different ranges of contractions mediated by RhoA/Rho-associated kinase|J03=Changes in intracellular calcium concentrations}}
{{Family tree| | | | | | | | | | | | | | | |!| | | |!| | |`|-|v|-|'| | |!| | | | | | | | }}
{{Family tree| | | | | | | | | | | | | | | |!| | | |!| | |`|-|v|-|'| | |!| | | | | | | | }}
{{Family tree| | | | | | | | K01 | | | | | |!| |,|-|'| | | | K02 | | | |!| | | | | K03 | K01=Fibrocytes|K02=Lock step mechanism of cyclic and contractile events|K03=T-helper cell type 2 on site of injury}}
{{Family tree| | | | | | | | K01 | | | | | |!| |,|-|'| | | | K02 | | | |!| | | | | K03 | K01=Recruitement of fibrocytes in lungs|K02=Lock step mechanism of cyclic and contractile events|K03=T-helper cell type 2 on site of injury}}
{{Family tree| | | | | | | | |!| | | | | | |!| |!| | | | | | |!| | | | |!| | | | | |!| | }}
{{Family tree| | | | | | | | |!| | | | | | |!| |!| | | | | | |!| | | | |!| | | | | |!| | }}
{{Family tree| | | | | | | | L01 | | | | | | L02 | | | | | | L03 | | | |!| | | | | L04 | |L01=Upregulation of C-X-C chemokine receptor type 4 (CXCR4)<br>on fibrocytes and its ligand<br>CXCL12 (stromal cell-derived factor 1)|L02=Excess ECM production|L03=Exerting traction force|L04=Interleukin-13}}
{{Family tree| | | | | | | | L01 | | | | | | L02 | | | | | | L03 | | | |!| | | | | L04 | |L01=Upregulation of C-X-C chemokine receptor type 4 (CXCR4)<br>on fibrocytes and its ligand<br>CXCL12 (stromal cell-derived factor 1)|L02=Excess ECM production|L03=Exerting traction force|L04=Interleukin-13}}

Revision as of 20:09, 2 March 2018

==Classification Gastritis

Gastritis Etiology Gasstritis synonyms
Non-atrophic
  • Helicobacter pylori
  • Other factors

Superficial Diffuse antral gastritis (DAG) Chronic antral gastritis (CAG) Interstitial - follicular Hypersecretory Type B*

Atrophic Autoimmune
  • Autoimmunity

Type A* Diffuse corporal Pernicious anemia-associated

Multifocal atrophic Helicobacter pylori Type B*, type AB*
Dietary Environmental
Environmental factors Metaplastic
Special form Chemical Chemical irritation Reactive
  • Bile
  • Reflux
  • NSAIDs
  • NSAID
  • Other agents
  • Type C*
Radiation Radiation injury

Risk assessment table

Scoring criteria for risk assessment*
Scoring system Score Risk
IMPROVEDD Score[1] Predicted % VTE risk through 42 days
0 0.4%
1 0.6%
2 0.8%
3 1.2%
4 1.6%
5-10 2.2%
Predicted % VTE risk through 77 days
0 0.5%
1 0.7%
2 1.0%
3 1.4%
4 1.9%
5-10 2.75
IMPROVE score[2] Predicted % VTE risk through 3 months
0 0.5%
1 1.0%
2 1.7%
3 3.1%
4 4%
5-8 11%
Padua Score[3] < 4 Low risk for VTE
≥ 4 High risk for VTE
Caprini score[4] 0-1 Low risk of VTE
2 Moderate of VTE
3-4 High risk of VTE
≥ 5 Highest risk for VTE

Pathophysiology of ILD

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Tissue injury in lungs
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Epitehelial injury
 
 
 
 
 
 
 
 
 
Vascular injury
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Mast cells in lungs
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
LPA6, LPA2, and LPA4 receptors
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Decreased sFRP-1 (secreted frizzled-related protein 1) in fibroblasts
 
Secretes tryptase
 
Transforming growth factor (TGF)-β
 
 
 
 
Insulin-like growth factor (IGF) signalling
 
 
 
 
 
 
 
Reduced expression of angiogenic factors,
vascular endothelial growth factor (VEGF)
 
Elevation of angiostatic factors,
pigment epithelium-derived factor
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Wnt/β-catenin signalling pathway
 
PAR-2/protein kinase (PK)C-α/Raf-1/p44/42 signaling pathway
 
Upregulation of Egr-1 (early growth response protein 1)
 
IGF-binding protein 5 (IGFBP-5)
 
 
 
IGF-binding protein 3 (IGFBP-3)
 
 
 
 
 
 
 
 
 
Loss of endothelial barrier function
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Dysregulation of repair in lung tissue
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Regulates transforming growth factor (TGF)-β
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Induction of syndecan-2 (SDC2)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Activation,proliferation, and migration of fibroblast to the site of injury
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Fibroblasts
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Altered PTEN (phosphatase and tensin homologue)/Akt axis
 
 
 
 
Acquire contractile stress fibres
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inactivates Fox (forkhead box) O3a
 
 
 
 
Protomyofibroblast,composed of cytoplasmic actins
 
Pleural mesothelial cells (PMCs)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Downregulation of cav-1 and Fas expression
 
 
 
 
De novo expression of α-SMA
 
TGF-β1-dependent mesothelial–mesenchymal transition
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Fibroblast resistant to apoptosis
 
 
 
 
 
 
Myofibroblasts
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Different ranges of contractions mediated by RhoA/Rho-associated kinase
 
 
Changes in intracellular calcium concentrations
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Recruitement of fibrocytes in lungs
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Lock step mechanism of cyclic and contractile events
 
 
 
 
 
 
 
 
 
T-helper cell type 2 on site of injury
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Upregulation of C-X-C chemokine receptor type 4 (CXCR4)
on fibrocytes and its ligand
CXCL12 (stromal cell-derived factor 1)
 
 
 
 
 
Excess ECM production
 
 
 
 
 
Exerting traction force
 
 
 
 
 
 
 
 
 
Interleukin-13
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Migration of fibrocytes to the site of injury
 
 
 
 
 
Tissue remodelling
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Alternate pathway activation of macrophages
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Lung Fibrosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

References

  1. . doi:10.1055/s-0037-160392910.1055/s-0037-1603929. Missing or empty |title= (help)
  2. Spyropoulos AC, Anderson FA, Fitzgerald G, Decousus H, Pini M, Chong BH; et al. (2011). "Predictive and associative models to identify hospitalized medical patients at risk for VTE". Chest. 140 (3): 706–14. doi:10.1378/chest.10-1944. PMID 21436241.
  3. Barbar S, Noventa F, Rossetto V, Ferrari A, Brandolin B, Perlati M; et al. (2010). "A risk assessment model for the identification of hospitalized medical patients at risk for venous thromboembolism: the Padua Prediction Score". J Thromb Haemost. 8 (11): 2450–7. doi:10.1111/j.1538-7836.2010.04044.x. PMID 20738765.
  4. Caprini JA, Arcelus JI, Hasty JH, Tamhane AC, Fabrega F (1991). "Clinical assessment of venous thromboembolic risk in surgical patients". Semin Thromb Hemost. 17 Suppl 3: 304–12. PMID 1754886.