Transcript No Slide Title

5. Lupus anticoagulant:
Antiphospholipid antibody syndrome
- Characterized by
1.Recurrent thrombosis
2. Recurrent abortions
3. Cardiac valve vegetations
4. Thrombocytopenia
- Associated with autoantibodies directed
against anionic phospholipids (cardiolipin )
- In vivo these antibodies induce
hypercagulability by inducing direct
platelet activation or interference with
production of PGI2 from endothelium
- Primary antiphospholipid antibody
syndrome----no associated autoimmune
disease
- Secondary antiphospholipid antibody
syndrome---patients have autoimmune
diseases such as systemic lupus
erythematosus
B. Low Risk for thrombosis
1.Hyperestrogenic states such as pregnancy
and Oral contraceptive pills that cause Increase
Synthesis of coagulation factors and decreases
synthesis of antithrombin 3
2.Aging: Increase platelets aggregation and
Decrease PGI 2 release by endothelium.
Morphology of thrombi
Thrombi can develop anywhere in the
cardiovascular system
- Arterial or cardiac thrombi:
- typically begin at sites of endothelial injury
or turbulence
Venous thrombi:
- Grow in direction of blood flow at site of
stasis.
 Thrombi are focally attached to the underlying vascular
surface
 - Arterial thrombi tend to grow in retrograde direction
from the point of attachment
- Venous thrombi extend in the direction of blood flow,
 The propagating portion of a thrombus tends to be
poorly attached and therefore prone to fragmentation ,
generating an embolus
 Thrombi grossly and microscopically have
laminations called Lines of Zahn , these lamination
represent pale layers of fibrin and dark layers of
RBCs.
 Lines of Zahn are well developed in arterial thrombi
 Thrombi in veins and some arteries don’t show
lines of Zahn but careful examination shows illdefined laminations.
 Thrombi in cardiac chambers or in aortic lumen
are not occlusive (Mural thrombi )
 Arterial thrombi are
1.Usually occlusive,
2. Gray white and firmly adherent.
coronary arteries
Cerebral arteries
Femoral arteries
Venous thrombi (phlebothrombosis)
1.Always occlusive
2. Red in color
3. Occur in lower limbs in 90% of cases
4.Rarely in: Upperlimbs, Periprostatic
plexus, ovarian & periuterine, Dural sinus,
Portal vein and Hepatic vein.
 Postmorteum clots can be mistaken at autopsy for venous
thrombi
• Fate of thrombi
1. Propagation- thrombi accumulate additional
platelets and fibrin
2. Embolization- thrombi dislodge or fragment and
aretransported elsewhere in the circulation
3. Dissolution occurs in recent thrombi
4. Organization and recanalization
5. Embolism:
- An embolus is a detached intravasular
solid, liquid or gaseous material that is
carried by blood from site of origin to
distant sites
• Types
1.99% due to dislodged thrombus, so
called Thromboembolism
- Other types
2. Fat embolism
3. Air embolism
4. Cholesterol emboli or atheroemboli
5. Amniotic fluid embolism
1. Systemic thromboembolism
- Emboli traveling within the arterial circulation
- 80% originate from intracardiac mural thrombi
- 2/3 Lt. ventricular myocardial infarction
- ¼ Lt. atrial dilatation
- Ulcerated atherosclerotic plaque,
- Aortic aneurysm
- Valvular vegetations
- The major site of lodgment of systemic
emboli:
1. Lower limbs 75%
2. Brain 10%
3. Intestine
4. Kidneys
5. Spleen
2. Plumonary thromboembolism
- 95% originate from deep veins of Lower
limbs
- Paradoxical embolus: Passage of an
embolus from venous to systemic circulation
through Interatrial defect (IAD) or
Interventricular defect, IVD
- Clinical consequence:
a. Organiztion: 60 – 80 %
b. Sudden death, Right ventricle failure( acute cor
pulmonale, Cardiovascular collapse when more than
60 % of pulmonary vessels are obstructed.
- Such as Saddle emboli
c. Pumonary hemorrhage: obstruction of medium sized
arteries in previously healthy individuals.
d. Pulmonary infarction: in patients with pulmonary
emboli in the medium sized arteries who have
history of left cardiac failure (Sluggish Bronchial
circulation)
d. Pulmonary Hypertension and right ventricular
failure due to multiple emboli.
3. Fat embolism
- Causes
1. Skeletal injury
2. Adipose tissue Injury
- In skeletal injury fat embolism occurs in 90%
of cases, but only 10% or less have clinical
findings:
a. Pulmonary Insufficiency
b. Neurologic symptoms
c. Anemia
d. Thrombocytopenia
e. Death in 10% of the cases
- Symptoms appears 1-3 days after injury
Tachypnea
Dyspnea
Tachycardia
Neurological symptoms
4. Air Embolism
-Gas bubbles within the circulation can obstruct
vascular flow (and cause distal ischemic injury)
- Generally, more than 100 mL of air are required to
produce a clinical effect
-
Air may enter the circulation
a. During obstetric procedures or
b. as a consequence of chest wall injury.
c. A particular form of gas embolism, called
decompression sickness, occurs when
individuals are exposed to sudden changes in
atmospheric pressure
- Deep-sea divers, and underwater construction workers are at
risk.
- When air is breathed at high pressure (e.g., during a deep-sea
dive), increased amounts of gas (particularly nitrogen) become
dissolved in the blood and tissues.
- If the diver then ascends (depressurizes) too rapidly, the
nitrogen bubbles out of solution in the blood to form gas
emboli that can induce focal ischemia in a number of tissues,
including brain and heart.
a- The rapid formation of gas bubbles within skeletal muscles
and supporting tissues in and about joints is responsible for
the painful condition called the bends
b- In the lungs, gas bubbles in the vasculature cause edema,
hemorrhages, leading to respiratory distress, called the
chokes. .
- Treating acute decompression sickness requires placing the
affected individual in a compression chamber to increase
barometric pressure and force the gas bubbles back into
solution.