Bi i 11: 



clotting factors of the blood has been <!• 



corpuscles and the platelets are normal in nun 



cium salts are normal, and, as Bowel] hi 



antithrombin. < me significant fai 



thromboplastin or of its active ingredient, kephalii 



clotting time of tin- blood when it is removed bj I 



menl with this observation it has been found that 



much in..!-.- rapidly, indeed sometimes in the usual • 



flow over cu1 or damaged tissue ami s,, become mi: ith thi 



tin. These facts taken together would Beem to i 



must lie in a deficiency in prothrombin, and 



from the platelets, which however arc nol «!• ■! in nun, 



further assume that these elements have und 



change preventing their disintegration. An accompanying in 



their agglutinating properties would at the same tim< 



ure in hemophilia to clump together at the site of 1 



to block the smaller vessels with thrombi; I 



time even alter clotting has iurred. 



Thrombus Formation 



The lirst formed portion of a thrombus is paler than l 

 ause it contains excessive numbers of platelets 

 that it is by a'_ r, _ r lut inatiuu of these inl hich tl 



blood vessels and by disintegrati g thrombin and th- 



plastin, that the dotting starts. This platelet agglutination i: 

 from stagnation in the bloodflow, <•!• from rougheni 

 vessel walls. Stagnation may \«- due eitl failure of tl 



as a whole as in heart < ii^. ■■ \,, local physical alt. 



cular tube, Betting up conditions in which eddj curr< 



Is of hi 1 an- formed, BUCh as will I., 



Buddenly become wider, as in var 

 sudden bend of large \ eins The flrsl 

 lowed by one ..t* a darker color, which ftlU 

 anastomotic branch. Similar s1 tion m 

 tion < • .- 1 u ^ . ■ ■ 1 bj lodgm< iboli in t ; 



bodies in tine suspension, bacteria, etc 

 very small ami o particularly in the 



ami lung's. The small thrombi 

 spreads into the larger vea 



in th agulabilit) of the bl W 



Bible that excessive amo 



this neutralizes the antithrombin in I»1<»<m1 m 



