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HEMODYNAMIC DISORDERS &

BLOOD VESSEL
PATHOLOGY

dr. Jessy Chrestella, M.Ked(PA), Sp.PA


Departemen Patologi Anatomi
Fakultas Kedokteran USU
Normal fluid homeostasis :
vessel wall integrity
maintenance of intravascular pressure
osmolarity within physiologic ranges.

Hemodynamic disorders

edema hemorrhage thrombosis

embolism infarction shock


EDEMA
increased fluid in the interstitial tissue spaces.

Ascites Hydrothorax

Anasarca Hydro-
pericardium

Figure 1. Pulmonary edema. A patient with congestive


heart failure shows pink-staining fluid in the alveoli.
(Rubin)
Pathophysiology of Edema
Reduced Plasma Osmotic Pressure
Increased Hydrostatic Pressure
(Hypoproteinemia)
Impaired venous return
Nephrotic syndrome
Congestive heart failure
Liver cirrhosis
Constrictive pericarditis
Malnutrition Protein-losing
Liver cirrhosis gastroenteropathy
Venous obstruction/
Lymphatic Obstruction
compression
Thrombosis Inflammatory
External pressure (e.g., Neoplastic
mass) Postsurgical /Postirradiation
Lower extremity inactivity Sodium Retention
with prolonged Excessive salt intake
dependency Increased tubular reabsorption of
Arteriolar dilation sodium
Heat Renal hypoperfusion
Neurohumoral Increased RAA secretion
dysregulation
Inflammation
Acute/Chronic
HYPEREMIA AND CONGESTION
Indicate local increased volume of blood in a
particular tissue.
Normal

Hyperemia active process


redder

Congestion passive process


cyanosis.
HEMORRHAGE
Extravasation of blood due to vessel rupture.
Discharge of blood out of the vascular compartment.

Hematoma:Hemorrhage into soft tissue. Such collections of


blood can be merely painful, as in a muscle
bruise, or fatal, if located in the brain.
Hemothorax: Hemorrhage into the pleural cavity.
Hemopericardium: Hemorrhage into the pericardial space.
Hemoperitoneum: Bleeding into the peritoneal cavity.
Hemarthrosis: Bleeding into a joint space.
Purpura: Diffuse superficial hemorrhages in the skin, up to 1
cm in diameter.
Ecchymosis: A larger superficial hemorrhage in the skin.
Petechiae: Pinpoint hemorrhages, usually in the skin or
conjunctiva.
EVOLUTION of HEMORRHAGE

ACUTE CHRONIC
PURPLE GREEN BROWN
HGB BILIRUBIN HEMOSIDERIN
Thrombosis
Formation of a thrombus, an aggregate of
coagulated blood containing platelets, fibrin,
and entrapped cellular elements, within a
vascular lumen.
Thrombus should be distinguished from a
simple blood clot.
The pathogenesis of thrombosis involves 3
factors:
Damage to endothelium
Alterations in blood flow
NORMAL OF BLOOD VESSEL

The vascular wall


A. Cross-section from a muscular artery (e.g., coronary artery)

6/24/2016 Departemen Patologi Anatomi FK USU Medan 13


Degenerative Disease of the Vessel
1. Atheroma
2. Arteriosclerosis

Atheroma Normal Arteriosclerosis


Deposition of yellow lipid Tunica intima Generalised
material in plaque under Tunica elastica degeneration
the intima Tunica media media
Tunica adventitia

14
THROMBOSIS
Virchows TRIANGLE
ENDOTHELIAL
INJURY

ABNORMAL FLOW HYPER-


(NON-LAMINAR) COAGULATION
ENDOTHELIUM
ANTI-Platelet PROPERTIES
Protection from the subendothelial ECM
Degrades ADP (inhib. Aggregation)
ANTI-Coagulant PROPERTIES
Membrane HEPARIN-like molecules
Makes THROMBOMODULIN Protein-C
TISSUE FACTOR PATHWAY INHIBITOR
FIBRINOLYTIC PROPERTIES (TPA)
ENDOTHELIUM
PROTHROMBOTIC PROPERTIES
Makes vWF, which binds PlatsColl
Makes TISSUE FACTOR (with plats)
Makes Plasminogen inhibitors
ABNORMAL FLOW
NON-LAMINAR FLOW
TURBULENCE
EDDIES
STASIS
DISRUPTED ENDOTHELIUM
ALL of these factors may bring platelets
into contact with endothelium and/or
ECF

1 HYPERCOAGULABILITY
(INHERITED)
COMMONEST: Factor V and Prothrombin defects
Common: Mutation in prothrombin gene,
Mutation in methyltetrahydrofolate gene
Rare: Antithrombin III deficiency, Protein C
deficiency, Protein S deficiency
Very rare: Fibrinolysis defects

2 HYPERCOAGULABILITY
(ACQUIRED)
Prolonged bed rest or immobilization
Myocardial infarction
Atrial fibrillation
Tissue damage (surgery, fracture, burns)
Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis)
Prosthetic cardiac valves
Disseminated intravascular coagulation
Heparin-induced thrombocytopenia
Antiphospholipid antibody syndrome (lupus anticoagulant syndrome)
Lower risk for thrombosis:
Cardiomyopathy
Nephrotic syndrome
Hyperestrogenic states (pregnancy)
Oral contraceptive use
Sickle cell anemia
Smoking, Obesity
MORPHOLOGY
ADHERENCE TO VESSEL WALL
HEART (MURAL)
ARTERY (OCCLUSIVE/INFARCT)
VEIN
OBSTRUCTIVE vs. NON-OBSTRUCTIVE
RED, YELLOW, GREY/WHITE
ACUTE, ORGANIZING, OLD
MURAL THROMBI, HEART
FATE of THROMBI
PROPAGATION (Downstream)
EMBOLIZATION
DISSOLUTION
ORGANIZATION
RECANALIZATION
OCCLUSIVE ARTERIAL THROMBUS
Embolism
The sudden blockage of the venous or arterial
circulations by any material that can lodge in
a blood vessel and obstruct its lumen.
Thromboembolus >>>

Figure 2. Pulmonary
embolism. The main
pulmonary artery and its
bifurcation have been
opened to reveal a large
saddle embolus.
ATHEROEMBOLI
CHOLESTEROL clefts are components of
atherosclerotic plaques, NOT thrombi!!!
EMBOLISM

Pulmonary
Systemic (Mural Thrombi and
Aneurysms)
Fat
Air
Amniotic Fluid
Infarction
Infarction is the process by which coagulative necrosis
develops in an area distal to the occlusion of an end
artery.
Pathology : The gross and microscopic appearance of an
infarct depends on its location and age.
Upon arterial occlusion, the area supplied by the vessel
rapidly becomes swollen and deep red.
Microscopically, vascular dilation and congestion and
occasionally interstitial hemorrhage are noted.
Figure 4. Spleen infarcts. A cut section of
Figure 3. Red infarct. A sagittal spleen displays multiple pale, wedge-
slice of lung shows a shaped infarcts beneath the capsule.
hemorrhagic infarct in upper
segments of the lower lobe.
SHOCK
Pathology of Vessels

Congenital Anomalies

Arteriosclerosis

HTN
Vasculitis ( inflammations)

Aneurysms & Dissections

Veins & Lymphatics

Tumors
ARTERIOSCLEROSIS
Thickening and hardening of the
arteries.

Hyaline arteriosclerosis (senility,


hypertension, diabetes mellitus)
Mnckebergs medial calcific sclerosis
: calcification on tunica media
Atherosclerosis : lipid deposition under
the intima
ATHEROSCLEROSIS
Large and medium-sized arteries
Intimal smooth muscle cell and lipid
accumulation
Irregular thickening of the wall and
narrowing of lumen
Major complications - ischaemic heart
disease, myocardial infarction, stroke,
gangrene of extremities
>50% of annual mortality in the US
1 cause of death in the UK
Geographic and racial variations
RISK FACTORS
NON MODIFIABLE MODIFIABLE
Age middle to Hyperlipidaemia
late HDL/LDL ratio
Sex Males, Hypertension
complications Smoking
Genetic Diabetes mellitus
Family history Life style, diet,
exercise
Coronary atherosclerosis
Normal (Lt.) and atherosclerotic
(Rt.) coronary arteries
Thrombosed atheromatous
plaque
ATHEROSCLEROSIS - COMPLICATIONS

Acute occlusion- ischaemic


necrosis
Chronic occlusion- atrophy
Aneurysm formation
Embolism
Thrombosed
coronary
atheromatous
plaque with
apical
myocardial
infarct
VASCULAR PATHOLOGY IN
HYPERTENSION
Accelerates atherogenesis
Potentiates aortic dissection and
cerebrovascular haemorrhage
Small vessel changes are typical;
especially in the kidneys
Hyaline arteriolosclerosis
Hyperplastic arteriolosclerosis and
fibrinoid necrosis
VARICOSE VEINS AT OTHER SITES

Haemorrhoids
Oesophageal Varices
Varicocele
DEEP VEIN THROMBOSIS

Thrombophlebitis

Phlebothrombosis
VASCULAR TUMOURS AND
TUMOUR-LIKE LESIONS
1. BENIGN
2. BORDERLINE/
Haemangioma INTERMEDIATE
Granuloma Haemangioendothelioma
pyogenicum
Vascular ectasia 3. MALIGNANT
Glomus tumour Angiosarcoma
Haemangiopericytoma
Kaposis sarcoma
Thank you

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