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

local anemia 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

ThrombosisDef.:

intravital intravascular blood clotting

Range:parietalobturative

Haemostasis1. 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 autolysis protein

activation thrombin liberation no platelet thrombus fibrinogen - fibrin non adherent elastic

intravital platelet based adherent to the

vessel wall friable /crumbly

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/mm3)

– thromboplastin liberation (e.g. following pancreas and lung surgery)

– endotoxin - DIC

– amniotic fluid embolism

– contraceptives……

Hypercoagulationinbornmutations with increased

levels of thrombocytes or lack of anticoag. proteins

acquired pregnancy contraceptives disseminated

neoplasms 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

EmbolismDef.:

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 amniotic fluid

life threatening

Embolism – Fate CELLULAR lysis trophoblastic progression

neoplastic METASTASES

bacterial metastatic sepsis

Caisson Disease (Decompression thickness – gas

microembolism)

divers

underwater construction workers

unpressurized aircraft in high altitudes

life threatening

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:

– external

– internal

Source:

– arterial

– capillary

– venous

Hemorrhage - pathogenesisHaemorrhagia

– per rhexin (trauma – tear of the vessel wall)

– per diabrosin (arosion – ulcus,

neoplasm)

– per diapedesin (increased vessel permeability- leakage)

Haemostasis1. 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 StatusesThrombocytopaties

thrombocytopenia, thrombasthenia

Coagulopatieshemofilia, hypoprothrombinemia,

afibrinogenemia, Vasculopaties

scurvy, m. Osler, m. Schönlein – Henoch