-
Anasarca
sever systemic edema
-
Most common cause of systemic edema
- CHF
- Increased venous hydrostatic pressure
-
most important cause of protein urea
nephrotic syndrome
-
lymphatic obstruction
blocks removal of extra fluid
-
hypoproteinurea
- edema is worse
- seen in periorbitals
-
increased blood flow into a tissue
hyperemia
-
impared outflow
congestion
-
lung congestion
with left heart failure
-
liver congestion
with right heart failure
-
central lobular necrosis
- last to receive blood
- occurs with hypo perfusion
-
hamatoma
hemorrhage within a tissue
-
-
-
-
permanent plug
thrombin and fibrin
-
Bernard soulier syndrome
defective gp-Ib
-
ADP on platelets
changes gp IIIa/IIb to bind to fibrinogen
-
Glanzmann thrombasthia
- gp IIIb/IIa deficency
- cant bind fibrin or other platelets
-
primary vs secondary plug
- primary only plts
- secondary plts and fibrin
-
AT3 inhibits
2, ,9,10,11,12
-
-
Virchows triad
- endothelial injury
- alterations of normal blood flow
- hypercoagulability
-
turbulent blood flow
brings platelets into contact with the endothelium
-
oral contraceptives and pregnancy
hypercoagulable because of increase in factor production
-
Antiphospholipid syndrom
patients have antibodies against phospholipids that can activate platelets or inactivate protein C
-
mural
non occlusive thrombi
-
sites of arterial thrombi formation
athroscletotic plaques and turbulent areas of vessel bifurcation
-
extension of plaques
- arterial grom retrograde
- venous grow antegragede
-
pre death vs post death thrombus
lines of zahn layers of pale thrombin and fibrin with lines of dark blood cells
-
thrombus on a heart valve
vegitation
-
verrucous endocarditis
- aka libman sacks
- patients with lupus erythematosus
- circulating immune complexes
-
Fate of a thrombus
- propagation, causing obstruction
- embolism
- dissolution
- organazation and recanalization
-
superficial venous thrombi
saphanous vein
-
deep venous thrombi
femoral vein
-
most venous emboli
are asymptomatic and not found till after the embolize
-
Trousseau syndrome
embolism form molignancy
-
systemic thromboembolism
usually form a mural clot in the left heart, on a valve or aorta
-
fat embolus
- second leading cause behind thromboembolis
- 1-3 days after injury
- fatty release is toxic to endothelium
-
caisson disease
more chronic decompression sickness
-
Infarction
- area of ischemic necrosis caused by occlusion of either arterial 97% or venous
- venous is usually congestion
-
Red infarts
- venous occlusion
- loose tissue; lungs
- duel circulations
- preveous congestion
- site of repercussion
-
white infarct
end arterial circulation
-
histological characteristic of infarction
- coagulative necrosis
- exception os the brain; liquefaction necrosis
-
septic infarts usually become and abscess
-
slow developing occlusions
- are less likely to infarct
- more time to develop alternative circulation
-
septic shock
- increased cadiac output due to arterial dilation
- mostly gram negative bacteria; endotoxins
- all effects from LPS
-
-
hypovelemic vs septic shock
- hypovolemic; cold skin
- septic; warm skin
|
|