digested blood in stool
coughed up blood
blood in vomit
blood in urine
focal pool of blood �balloon�
multiple tiny hemorrhages
like above but larger
blood clot in vessel
thrombus in motion, or any abnormal object floating in circulation
emboli too large for circulation
Necrosis due to emboli obstructing blood flow to or from and organ or tissue
Hypovolemic or normovolemic; ultimate result is hypotension, lock of O2 delivery; septic hypovolemic, anaphylactic, cardiogenic etc,
Increase blood flow into arterioles; normal or pathologic
blood stasis in the venules; due to
Basic ability of the body to maintain vessels and blood flow in the vessels
Interaction between blood vessel wall, platelets and coagulation factors.
4 Steps to Hemostsis:
1: Vasoconstriction2: Platelets gather at site3: Coagulation Factor4: Return to Normal
What are the 2 Phases of coagualtion?
Mechanical and Chemical
Primary Hemostasis: Damage attacts platelets, attach to each other and endothelium to prevent more damage
Secondary and Tertiary Hemostasis: Platelets Initiate, Coagulation Cascade
What are the 3 Pathways of the Coagulation Cascade?
Intrinsic, Extrinsic, and Common
Intrinsic Pathway is AKA?
Contact Activation Pathway
Extrinsic Pathway is AKA?
Tissue Factor Pathway
-Stimulation by exposed collagen and/ or damage to vessel for platelets to adhere-Factors 5,7,9,10, and11
-Stimulated by non-vascular damage (releases fluids and chemicals)-Factors 7 and 10
-Goal: lots of Fibrinogen to fibrin-Intrinsic and Extrinsic Pathway come together at Foactor 10-Now activated Thrombin is a major coagulantFactor 5 and 8 together converts prothrombin to Thrombin
-XII activates XI-XI activates IX w/ help of calcium-IX (and VIII) activates X-X (and V) convert Prothrombin to Thrombin
-Tissue Factor released binds with and activates VII-Activated VII-TF catalyzed by C+++ activates X-X (and V) convert Prothrombin to Thrombin
-PPSC->Myeloid Stem Cell-> Megakaryoblast-> Promegakaryocyte-> Megakaryocyte-> Platelets -2-4 umInactive is smooth/ Active is irregular