FMS3 Path

• A) Non-infmalitory
•      ^ Hydrostatic Preassure
•     Decrease Onconic P
•     No change to vascular Perm

B) Inflamitory/ ^ vascular Perm/direct Vasc dmg

Active!

• Arteriol Vasodil= ^ blood flow
• Red tissue/warmer

Passive

• Imparied outflow
• Cyanotic tissues

Congestion

A) Sudden Lv failure- ^ preasure- engorged capilary beds = transudate creation. Frothy pink edema thats soffocates

B) Persistent, less pressure. Aveolar walls respond by thickining. ^ macrophages heart failure cells

Congestion

• A) 2ndry to shock/hepatic vein thrombosis. Central vein/centrilobar hepatocytes distended w/ blood.
• Blood flows from Portal tract to central vein- centrilobar hepatocyts vulerable to hypoxic injury

B) RV failure. Centrilobar hepatocyt necrosis. Nutmeg liver

• 1) Exsposure to subendothelial collagen leads to platlet binding and activation
• 2) Platlets adhere and aggregate at injury site= primary platlet plug
• 3) @ same time, Activation Coag Casscade
• 4) Prothrombin converted to active form (thrombin) --> catalyses circulating fibrinogen to fibrin--> platlet plug

A) 2ndry to congestion & ^ preasure

B) Trauma/Atherosclerosis etc

* Excessive hemorage = jaundice due to release of bilirubin following redblood cell breakdown

• 1) Endothelial injury
• 2) Stasis or turbulent blood flow
• 3) blood hypercoaguability

MI/ hypertension/ hypoxia/ cigarette smoke/ Bacterial endotoxin/ radiation/ trauma-sugury/vasculitus

Cells/platlets in center, plasma normaly flow along vessel phriphery. Disruption of laminar flow increases chance of contact between platlets and vessel wall.

Result of Atherosclerotic vessel disease

turbulance arises at branch points- Aortic/iliac/carotid artery bifurcations

Common sites: Coronary/cerebral/femoral arteries.

More compact and pale than Venious. More platlets/fibrin/leukocytes. less RBC