GENERAL PATHOLOGY

1. Click to add Text

2. Click to add Text
Hemodynamic & circulatory
disorders - 1
Dr. Murali B M M.D (path)

3. HOMEOSTASIS
 “Tendency of the body to maintain vital parameters
at constant levels”
 Maintenance of Normal Homeostasis depends upon
(i) vessel wall integrity
(ii) intravascular pressure
(iii) osmolarity of blood
altered by
Fluid Imbalance Hemodynamic disturbances
(i) Edema (i) Hemorrhage (iii) Embolism
(v) Shock (ii) Thrombosis (iv) Infarction

4. Hemorrhage
Definition: Extravasation of blood due
to vessel rupture
1. Hematoma: accumulation of blood
within tissue.
2. Petechiae: Pinpoint hemorrhages
<2 mm in diameter seen in skin,
mucous membrane
3. Purpura: 2 to 10 mm in diameter
seen on skin
4. Ecchymosis: >10 mm in diameter
(bruises)
5. Large accumulations of blood in one
or another of the body cavities are
called hemothorax (in pleural cavity,
hemopericardium (pericardial
cavity), hemoperitoneum
(peritoneal cavity), or hemarthrosis
(in joints).

5. Hyperemia & Congestion
 Hyperemia : An active process resulting
from tissue inflow because of arteriolar
dilation. e.g. skeletal muscle during
exercise or at sites of inflammation. The
affected tissue is redder because of the
engorgement of vessels with
oxygenated blood.
 Congestion: A passive process
resulting from impaired outflow from a
tissue. It may be systemic e.g. cardiac
failure, or local e.g. an isolated venous
obstruction. The tissue has a blue-red
color (cyanosis), due to accumulation of
deoxygenated hemoglobin in the
affected tissues.

6. EDEMA
 Edema signifies increased fluid in the interstitial tissue
spaces.
 Depending on the site, examples of fluid collections are
hydrothorax , hydro pericardium and hydroperitoneum
(ascites).
 Anasarca: severe, generalized edema with profound
subcutaneous tissue swelling.
Types of edema:
 Transudate: protein poor (<3 gm/dl) fluid with specific
gravity of <1.012. mechanism is due to imbalances in
normal hemodynamic forces e.g. congestive heart failure,
liver and renal disease etc.
 Exudate -protein rich (>3 gm/dl) fluid with a specific gravity
of >1.020 results from endothelial damage and alteration of
vascular permeability e.g. inflammatory and immunologic

7. Pathophysiologic Categories of Edema
 Increased Hydrostatic Pressure
1.Venous obstruction
2.Congestive heart failure
3.Ascites(liver cirrhosis)
4.Lower extremity inactivity with prolonged dependency
 Reduced Plasma Osmotic Pressure
(Hypoproteinemia)
1.Protein-losing nephrotic syndrome
2.Liver cirrhosis (ascites)
3.Malnutrition
 Sodium Retention
1.Excessive salt intake with renal insufficiency
2.Increased renin-angiotensin-aldosteron secretion
 Lymphatic Obstruction Inflammation
1.Acute inflammation
2.Chronic inflammation

9. T h r o m b o s i s
 It is a process by which a thrombus is
formed.
 A thrombus is a solid mass of blood
constituents which develops in artery or
vein. It represents hemostasis in the
intact vascular system.
 Pathogenesis: Three primary factors
predispose to thrombus formation, the
so-called Virchow’s triad:
(1)endothelial injury
(2)stasis or turbulence of blood flow
(3)blood hypercoagulability

10. Figure : Virchow triad in thrombosis. Endothelial integrity is the single
most important factor. Note that injury to endothelial cells can affect
local blood flow and/or coagulability; abnormal blood flow (stasis or
turbulence) can, in turn, cause endothelial injury. The elements of the
triad may act independently or may combine to cause thrombus
formation.

11. Hypercoagulable States
 Primary (Genetic)
1. Mutation in factor V gene (factor V Leiden)
2. Mutation in prothrombin gene
3. Mutation in methyltetrahydrofolate gene
4.Antithrombin III deficiency
5.Protein C deficiency
6.Protein S deficiency
7. Fibrinolysis defects

12. Hypercoaguable States
 Secondary (Acquired)
High risk for thrombosis
1.Prolonged bed rest or immobilization
2.Myocardial infarction, Atrial fibrillation
3.Tissue damage (surgery, fracture, burns)
4.Cancer
5.Prosthetic cardiac valves
6.Disseminated intravascular coagulation
Lower risk for thrombosis
Hyperestrogenic states (pregnancy), Oral
contraceptive use, Sickle cell anemia, Smoking.

13. Morphology of thrombus
 Thrombi may develop anywhere in the
cardiovascular system, the cardiac
chambers, valve cusps, arteries, veins,
or capillaries.
 They vary in size and shape,
depending on the site of origin.
 When arterial thrombi arise in heart
chambers or in the aortic lumen, they
usually adhere to the wall of the
underlying structure and are termed
mural thrombi .
 Mural thrombi have laminations, called
lines of Zahn ; these are produced by
alternating pale layers of platelets
admixed with some fibrin and darker
layers containing more red cells.

14. Arterial (or cardiac) thrombi
 Usually begin at a site of
endothelial injury (e.g.,
atherosclerotic plaque) or
turbulence ( near vessel
bifurcation).
 Common sites are coronary,
cerebral, and femoral arteries.
 Usually firmly adherent to the
arterial wall and are gray-white and
friable (white thrombi), composed
of a tangled platelets, fibrin,
erythrocytes, and degenerating
leukocytes.
 Arterial thrombi grow in a retrograde
direction from the point of
attachment and can fragment,
creating an embolus.

15. Venous thrombosis
 Venous thrombi characteristically
occur in sites of stasis.
 Most commonly (90%) affects the
lower limbs veins.
 thrombi contain more enmeshed
erythrocytes and are therefore
known as red, or stasis thrombi
.
 Venous thrombi extend in the
direction of blood flow (i.e.,
toward the heart) and can
fragment, creating an embolus .

16. Thrombi on Heart Valves
Thrombi on heart valves are Called
vegetations.
Causes of vegetations:
1. infective endocarditis : Bacterial
or fungal blood-borne infections
2. nonbacterial thrombotic
endocarditis Sterile vegetations.
3. noninfective , verrucous (Libman-
Sacks) endocarditis in systemic
lupus erythematosus

17. Fate of thrombus