This document outlines a lecture plan on local blood circulation disorders. It discusses various types of disorders including arterial hyperemia, venous hyperemia, ischemia, stasis, thrombosis, and embolism. For each disorder, it provides definitions and discusses etiology, pathogenesis, clinical manifestations, and consequences. It also lists some suggested reading materials and includes diagrams on anatomy of local blood circulation and classifications of arterial hyperemia.

1. KHARKIV INSTITUTE OF MEDICINE AND
BIOMEDICAL SCIENCES
LOCAL BLOOD
CIRCULATION DISORDERS
2021-2022
Lector: DM, Ass. Professor
Valeriia V. Hnatiuk

2. PLAN OF LECTURE
1. Arterial hyperemia: definition, etiology, pathogenesis, clinical
manifestations, consequences.
2. Venous hyperemia: definition, etiology, pathogenesis, clinical
manifestations, consequences.
3. Ischemia: definition, etiology, pathogenesis, clinical
manifestations, consequences.
4. Stasis: definition, etiology, pathogenesis, clinical
manifestations, consequences.
5. Thrombosis: definition, etiology, pathogenesis, clinical
manifestations, consequences.
6. Embolism: definition, etiology, pathogenesis, clinical
manifestations, effects.

3. Suggested Reading
1. Pathophysiology : textbook / N.V. Krishtal, V.A. Mikhnev, N.N.
Zayko et al. ; edited by N.V. Krishtal, V.A. Mikhnev. – 3rd edition.
– Kiev : AUS Medicine Publishing, 2019. – 656 p.
2. Pathophysiology : textbook / N.K. Simeonova; edited by V.A.
Mikhnev. –2d edition. – Kiev : AUS Medicine Publishing, 2015. –
544 p.
3. Essentials of Pathophysiology / Carol M. Porth. – 4th edition. –
Wolters Klumer, 2015. – 1247 p.
4. General and clinical pathophysioilogy/ Editer by Anatoliy V.
Kubyshkin. – Vinnytsa : Nova Knyha Publishers, 2016. – 656 p.

4. Anatomy of local blood circulation

5. Types of local blood circulation disorders
ARTERIAL HYPEREMIA VENOUS HYPEREMIAA
ISCHEMIA STASIS
THROMBOSIS EMBOLISM

6.  It is local increasing of blood supply due to
excessive blood inflow through arterial vessels
ARTERIAL HYPEREMIA

8. Classification of arterial hyperemia
Active (working)
hyperemia
(organ
hyperfunction)
Reactive
hyperemia
(after short-term
construction)
Physiological
arterial
hyperemia
Pathological
arterial
hyperemia
Neurogenic
arterial
hyperemia of
neurotonic type
Neurogenic arterial
hyperemia of
neuroparalytic type
Neurogenic
arterial
hyperemia
Metabolic
arterial
hyperemia

10. Neuroparalytic arterial hyperemia
Claude Bernard's experience (1851)
right cervical sympathetic knot was removed

13. Clinical signs:
 redness,
 increase local temperature,
 dilatation of small arteries, arterioles, veins and capillaries,
 increase of the pressure in arterioles, capillaries and veins,
 pulsation of small veins and capillaries,
 increase of the tissue volume,
 intensifying of metabolism and organ's function.

14. Consequences:
 positive – increased organ function and tissue metabolism
 negative - rupture of the vessel wall

15. It means decreasing of blood outflow from organs
and tissues due to inadequate venous drainage
VENOUS HYPEREMIA

16. Etiology:
► obstruction of veins by thrombus or an embolus –
intravascular factors;
► compression by tumor, cicatrix, enlarged uterus -
extravascular factors;
► pathology vein's walls – congenital (innate) and
acquired defects od structure of vascular wall of
venues;
► generalized disorder central blood circulation (heart
failure)

17. Clinical signs of venous hyperemia
 cyanosis,
 decrease local temperature,
 edema (swelling),
 enlarging of an organ or a region of tissue,
 increase of pressure in veins and capillaries in the
region of congestion,
 slowing of the blood flow,
 diapedesis of erythrocytes.

18. Ischemia is local blood violation, which develops
due to limitation or full lack of arterial blood inflow due
to constriction or occlusion of adducting arteries
Compression
ischemia appears as a
result of squeezing of
an artery by a ligature,
cicatrix, tumor,
foreign body, etc.
Obstruction
ischemia is a result of
a partial or complete
occlusion of an
artery's lumen by a
plaque, blood clot or
an embolus.
Angiospasmic ischemia due to
reflex spasm caused by
1) emotional factors (fear, pain);
2) physical factors (cold, injury);
3) chemical agents;
4) biological stimulants (toxins of
bacteria)

19. Clinical signs:
► paleness of the ischemic region or organ,
► decrease local temperature,
► pain,
► decrease of the tissue volume,
► disturbance of sensibility manifesting as parestesia
(feeling of numbness, tingling),
►decrease of the pressure in arterioles, capillaries and
veins

20. Consequences:
 disorders intracellular metabolism
 cell death - necrosis

21. Stasis – it is a decrease or stop of blood flow in the
capillars, small arterials and veins
true
(capillary)
stasis due to
pathologic
changes of
capillaries or
abnormality
of blood
reology
ischemic
stasis
due to stop
of blood
inflow
venous
stasis

22. PATHOGENESIS

24. Pale thrombi is
formed by platelets,
leukocytes and a small
amount of plasma
proteins
Thrombosis is a formation of clot, containing blood's elements
on the internal surface of vessels in a living organism
parietal
(partially decrease
vessel's lumen)
Mixed clots have
alternating white
and red layers.
Red thrombi
contains
erythrocytes
entrapped in
fibrin net
obstructive

26. Virchov's triad
1. Injury of a vessel's wall,
by physiologic factors
(mechanic injury, electric
current), chemical (NaCI,
FeCl3, AgNO3) and biologic
(bacteria's endotoxins) factors
2. Disturbance of the balance
between coagulation and
fibrinolytic systems.
3. Slowing of blood flow
and its abnormalities (turbulence in
the aneurysma region).

27. I. Cellular stage
(it takes some minutes)
aggregation platelets
(sticking to each other)
Changes of the membrane
potential of a vascular wall
and the charge of platelets
Injury of the vessels wall
Adherence (precipitation on
the injured surface of
vessels' endothelium
platelets' disintegration and
releasing of the platelet
coagulation factors
- thromboplastin

28. II. Plasma stage of coagulation
(it takes some hours)
Active thromboplastin
formation of active thrombin
thrombin catalyzes
transformation of
fibrinogen into fibrin
Formation a clot (formed net
contains various blood cells
(platelets, leukocytes,
erythrocytes)
III. Retraction (thrombostenin (retractozyme) causes contraction of
the fibrin fibers. The clot retracts and becomes denser.

29. is obstruction of blood or lymphatic vessels with bodies (emboli),
brought with blood or lymph
Exogenous:
• air,
• gas,
• foreign bodies,
• bacterial, parasitic
Endogenous:
• thrombotic (thromboemboli),
• fat,
• cellular, tissue
• amniotic fluid
EMBOLISM

30. The source of the thromboemboli is
a fragment of detached thrombus.
Fat embolus occurs due to
injury of the bone marrow,
subcutaneous or pelvic fatty
tissue, broken bones
Tissue embolus due to pieces of
tissues rich by water (bone
marrow, muscles, brain, liver,
trophoblast) enter in to the
circulatory system
Gas embolus is the basic pathogenic link of the state of
decompression, particularly caissons disease.

32. Thanks for attention
Be healthy!