General Pathology

Circulation
Disorders - II

Manifestations &
Causes of Local
Circulatory
Disturbances

Jaroslava Dušková
Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague
Manifestations of Local Circulatory
Disturbances

 local hyperemia
 local anemia

LOCAL ISCHEMIA
Manifestations of Local Circulatory
Disturbances

 local hyperemia
– active arterial (fluxe)
capillary (peristatic)
– passive venous (stasis)
 Manifestations of Local Circulatory
Disturbances

 local anemia
– slow development – vascular atrophy
– fast development – dystrophy , necrosis
Ischemia – stratification of changes

 complete necrosis - central part

 myomalacia
 hyperemia
 interstitial leucocyte infiltration – vital
reaction
 dystrophic steatosis (& glycogenosis)
 healthy
Causes of Local Circulatory
Disturbances
 localanemia
stenosis to occlusion of artery
 lumen embolism
 wall atherosclerosis, thrombosis
(spasmus, depositions,
inflammations, tumours)

 combination of previous
 neighbourhood compression
Causes of Local Circulatory
Disturbances
 local hyperemia
active
 function
 inflammatory vasodilation
passive (outflow blocade)
 lumen
 wall
 neighbourhood
Thrombosis
Def.:
intravital intravascular
blood clotting
Range:
parietal
obturative
Haemostasis
1. Endothelium damage – vWF secretion
2. Thrombocytes adhesion & aggregation
 Thrombocytes secretion
 serotonin, PDGF, thromboxan A2 vasoconstriction

 fibronectin, vWF, fibrinogen aggregation

3. Plasma factors - proteins synthesized in hct,

(vit. K dependence) cascade activation
 Coagulum x Thrombus

postmortem intravital
 autolysis protein  platelet based
activation  adherent to the
 thrombin liberation vessel wall
 no platelet thrombus  friable /crumbly
 fibrinogen - fibrin
 non adherent
 elastic
Types of Thrombi
 red stagnation
 white fluxe
 mixed
 hyaline
Thrombosis - causes
 blood stagnation
 endothelium damage
 blood composition
changes
Thrombosis - causes
 blood stagnation
– heart failure
– vein insufficiency
– local factors (compression)
laminar flow disturbance
Thrombosis - causes
 endothelium damage
– atherosclerosis
– inflammation
– injury
– hemodynamic stress
– high cholesterol levels
 Thrombosis - causes
 blood composition changes
– increased platelet number (over 400 000/mm 3)

– thromboplastin liberation (e.g. following

pancreas and lung surgery)
– endotoxin - DIC
– amniotic fluid embolism
– contraceptives……
 Hypercoagulation
inborn acquired
mutations  pregnancy
with increased  contraceptives
levels of
thrombocytes or  disseminated
lack of anticoag. neoplasms
proteins  atrial flutter
 arteficial valves
 surgery…….
Thrombus development
 no
 lysis
 organisation (decoloration,
recanalization, hyalinization,
dystrophic calcification - phlebolith)
 lysis + organisation
 embolism
 puriform softening
 infection
Natural Anticoagulant Systems

1. Antithrombins – e.g.antithrombin III

inhibits fcts IXa,Xa,XIa,XIIa

2. Proteins C, S (vit K dependent) – inh. fcts

Va, VIIIa

3. Plasminogene – plasmin system

fibrin breakdown
Embolism
Def.:
transport of a compact particle in
circulation with stopping in the
place of anatomic narrowing
Emboli – Types
 thrombotic
 fat
 air
 amniotic fluid
 cellular (neoplastic, bacterial
trophoblastic)
 foreign body
Embolism – Fate
THROMBOTIC
 no
 organisation
 lysis , resorption
 progression
 fat
 air life threatening
 amniotic fluid
Embolism – Fate
CELLULAR
 lysis trophoblastic
 progression
neoplastic METASTASES
bacterial metastatic sepsis
Caisson Disease
(Decompression thickness – gas
microembolism)
life threatening

 divers
 underwater construction workers
 unpressurized aircraft in high altitudes
Factors Influencing
Vessel Occlusion Result
 anatomy
 time
 tissue/organ sensitivity to
hypoxy
 functional status
 general circulation status
 MEDICAL INTERVENTION
Haemorrhagia
Def.:
blood extravasation

(and the presence of blood

in the tissue)
Hemorrhage – Classification
Localisation: Source:
– external – arterial
– capillary
– internal – venous
 Hemorrhage - pathogenesis
Haemorrhagia

– per rhexin (trauma – tear of the

vessel wall)
– per diabrosin (arosion – ulcus,
neoplasm)
– per diapedesin (increased vessel
permeability- leakage)
Haemostasis
1. Endothelium damage – vWF secretion
2. Thrombocytes adhesion & aggregation
 Th secretion
 serotonin, PDGF, thromboxan A2
vasoconstriction
 fibronectin, vWF, fibrinogen aggregation

3. Plasma factors - proteins synthesized in hct,

(vit. K dependence) cascade activation
Hemorrhagic Statuses
Thrombocytopaties
thrombocytopenia, thrombasthenia
Coagulopaties
hemofilia, hypoprothrombinemia,
afibrinogenemia,
Vasculopaties
scurvy, m. Osler,
m. Schönlein – Henoch