Page 93 - Concise Pathology for Exam Preparation ( PDFDrive )

78 SECTION I General Pathology

(e)
Infected valve disease
Prosthetic valves
(f)
Radiation injury
(g)
Chemical agents (smoking, hypercholesterolaemia, homocysteineamia, bacterial
(h)
toxins and endotoxins)
Alteration in normal blood flow (stasis or turbulence):
2.
is
Stasis typically seen hyperviscosity syndromes and polycythemia; whereas, turbu-
in
in
is
lence commonly associated with hypertension. Alterations normal flow result in:
(a)
of
Disruption laminar flow
of
Decreased
(b) hepatic clearance activated coagulation factors
to
Damage endothelium
(c)
3.
Conditions predisposing to hypercoagulability:
Genetic:
(a)
C
(i)
S,
Deficiency antithrombotic factors like AT III, proteins and Methylene
of
tetrahydrofolate reductase (MTHFR) gene mutation and defects fibrinolysis.
in
(ii)
V

Increased prothrombotic factors as in Factor mutation/factor Leiden

V

C

(activated protein resistance); prothrombin G20210A mutation (excessive

of
levels prothrombin); high levels factors VII, XI, IX, VIII, von Willebrand
of
factor and fibrinogen and homocysteinuria.
Acquired:
(b)
(i) Venous stasis: Prolonged immobilization and congestive cardiac failure

(ii) Increased platelet activation: Cancers, acute leukaemias, myeloproliferative

disorders, paroxysmal nocturnal haemoglobinuria, prosthetic cardiac valves, atrial
fibrillation, myocardial infarction and thrombotic thrombocytopenic purpura

(iv) Increased hepatic synthesis of coagulation factors or reduced anticoagulant

synthesis: Oral contraceptives, pregnancy, etc.

(v) Antiphospholipid syndrome

(vi) Tissue injury: Surgery, fracture and extensive burns
Q. Write briefly on the morphology of a thrombus.
Ans. Thrombi are grey-white, friable, tangled strands fibrin and platelets, which may
of
as
form anywhere the cardiovascular system, cardiac chambers, arteries and veins and
in
in
capillaries.
General Features of Thrombi
of
be
• �Different sizes and shapes thrombi may seen, dictated by:
of
• �Site origin
to
• �Circumstances leading their development
t
a
f
n
• �Cardiac thrombi mostly develop the regions turbulence and sites endocardial

o
f

i
o
o
injury (atrial appendages, endocardial surface myocardial infarct and cardiac valves).
f
a
of
• �Thrombi in cardiac chambers or the presence laminations lines of
or
aorta show
Zahn (paler layers fibrin and platelets alternating with darker layers RBCs).
of
of
veins do
of
• �Thrombi in smaller arteries or not show lines Zahn.
of
to
• �Mural thrombi are attached one wall an underlying structure, usually capacious

of
lumina heart chambers and aorta.
• �Arterial thrombi are usually occlusive when they involve smaller vessels; large vessels,

eg, iliac and common carotid tend have mural thrombi.
to
• �Venous thrombi (phlebothrombosis) are invariably occlusive and contain large RBC

a
a
component, because these are formed relatively static environment. These are also
in
of
called red or stasis thrombi. Other features venous thrombi are follows:
as
• �Lines Zahn are not well developed.
of
of
• �Mostly affect veins lower extremity (90% cases).
be
• �May confused with post-mortem clots.
• �Always have point attachment the underlying structure, firmest the point
o
t
t
o
f
f
a
a
o
origin.
to
of
• �Contraction thrombus gives way slit-like lumen which restores blood flow
a

a

of
to
leading propagation the thrombus upstream and downstream.
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