13. 3. Hemorrhage
arterial + venous + capillary
H. per rhexin – injury - brain
H. per diabrosin – erosion – peptic ulcer
H. per diapedesin – transmigration of RBC
(no damage of capillaries) – toxic injury +
stasis
14. 3. Hemorrhage - sequelae
1. loss volume
– > 20% hemorrhagic shock
2. loss rate
– acute hemorrhagic shock
– chronic (peptic ulcer, metrorhagia, colonic adenoCa)
iron deficiency anemia
3. site
– subcutaneous x brain
15. Disseminated Intravascular
Coagulation (DIC)
basis: widespread activation of thrombin
Mi: fibrin thrombi in microcirculation
1. stage
– multiple fibrin thrombi in microcirculation
consumption of PLT + coagulation proteins
2. stage
– fibrinolytic system activation serious
bleeding
29. Metastasis
similar to embolism x secondary focus is formed
hematogenous – sarcomas
lymphogenous – carcinomas
– regional LNs
– sentinel LN
porogenous – gastric and ovarian carcinomas
– through hollow organs, along serosas
30. 7. Ischemia / Infarction
= ischemic necrosis due to occlusion of
arterial supply (or venous drainage?)
causes:
– thrombotic or embolic events (99%)
– vasospasm, hemorrhage in AS plaque
– external compression (tumor)
– twisting (testicular + ovarian torsion, bowel
volvulus)
33. 7. Infarction
- morphology
wedge shape
– apex to occluded artery
– base to organ periphery
+ fibrinous exudate (pleuritis, pericarditis
epistenocardiaca)
onset – poorly defined, hemorrhagic
later – sharper margins + hyperemic rim
34. 7. Infarction
- morphology
ischemic coagulative necrosis – 3 zones
1. total necrosis - centre
– loss of nuclei, eosinophilia of cytoplasm, architecture is
preserved
2. partial necrosis
– some cells survive
– inflammation (neutrophils) – 1-2 day degradation of
dead tissue
3. hyperemic rim