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==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		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		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	< 4	Low risk for VTE
	≥ 4	High risk for VTE
Caprini score	0-1	Low risk of VTE
	2	Moderate of VTE
	3-4	High risk of VTE
	≥ 5	Highest risk for VTE

Pathophysiology of ILD

Algorithm showing pathophysiology of Interstitial Lung Disease

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-β (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-β (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 caveolin-1 (cav-1) and Fas expression

De novo expression of α-smooth muscle actin (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 extracellular matrix production

Exerting traction force

Interleukin-13

Migration of fibrocytes to the site of injury

Tissue remodelling

Alternate pathway activation of macrophages

Lung Fibrosis