Pathology of thrombosis

1. TOPIC: Thrombosis & SHOCK
PREPARED BY: DR.RATHER ALI MOHMAD
SEMEY STATE
MEDICAL
UNIVERSITY

2. PLAN OF LECTURE
 INTRODUCTION
 TYPES
 MECHANISM OF THROMBOSIS
 PATHOGENESIS
 CAUSES
 SHOCK
 TYPES
 PATHOGENESIS
 CONCLUSION

3. Thrombosis
 is the process of a blood clot, also known as a
thrombus, forming in a blood vessel. This clot can
block or obstruct blood flow in the affected area, as
well as cause serious complications if the clot moves to
a crucial part of the circulatory system, such as the
brain or the lungs.

4. It is normal for the body to produce clotting factors like platelets
and fibrin when a blood vessel is injured, to prevent an excessive
loss of blood from the body. If this effect is over productive it can
obstruct the flow of blood and form an embolus that moves
around the blood stream

5. Thrombosis Types
 Thrombosis can be broadly classified as either:
 venous thrombosis or
 arterial thrombosis, according to where the thrombus
presents in the body.

6. according to where it occurs
including:
 Deep vein thrombosis
 Portal vein thrombosis
 Renal vein thrombosis
 Jugular vein thrombosis
 Budd-Chiari Syndrome
 Paget-Schoetter disease
 Cerebral venous sinus thrombosis

7.  Renal vein thrombosis
 The renal vein can also be obstructed by a thrombus, which
can result in reduced kidney drainage. This type is known as
renal vein thrombosis and is common in patients with
nephrotic syndrome.

8.  Jugular Vein Thrombosis
 Thrombosis of the jugular vein is an extremely rare
type of venous thrombosis that usually occurs as a
result of intravenous drug use but is also associated
with infection and malignancy. Individuals affected by
this type may develop serious complications such as
systemic sepsis, pulmonary embolism and
papilledema.

9. Budd-Chiari Syndrome
This type of venous thrombosis involves the obstruction
of the hepatic vein and the outflow of blood from the
liver. It is uncommon but may be recognized by
symptoms of abdominal pain, ascites and hepatomegaly.

10. Paget-Schroetter Disease
Also known as effort thrombosis, this refers to
thrombosis occurring in an upper extremity vein, such
as the axillary or subclavian vein. It usually affects
physically active people and presents most often
immediately after or during high-intensity exercise.

11.  Cerebral Venous Sinus
Thrombosis
 This is a rare type of stroke,
caused by a thrombus in the
venous channels of the
brain. It is characterized by
headache, abnormal vision
and symptoms of stroke,
such as difficulty speaking
and moving the facial and
arm muscles. The majority
of people make a full
recovery, but adequate
treatment as for a stroke is
required to promote healthy
recovery.
 Thrombotic Stroke
 This is a type of arterial
thrombosis that involves a
blockage in the cerebral
artery that is responsible
for supply blood and
oxygen to the brain.
Thrombotic stroke usually
presents more gradually
than other types of stroke,
such as hemorrhagic, due
to the gradual build up of
the thrombus and the
growing obstruction

12. Venous Thrombosis
 Deep vein thrombosis
 (DVT) commonly involves the formation of a blood clot in the femoral
vein of the leg and is the most common type of thrombosis to cause
serious complications. If the thrombus breaks off to form an embolism it
moves with the blood towards the lungs and commonly causes
pulmonary embolism
 Typical signs of deep vein thrombosis are pain, swelling and redness in
the legs. If these are noted and DVT is suspected, assessment and
management should be conducted as soon as possible to reduce the
possibility of pulmonary embolism.

13. cause portal hypertension and affect the blood supply to the liver.
In most cases, it results from other abnormalities in the body, such
as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.

14.  Arterial thrombosis, also known as atherothrombosis
due to its association with atheroma rupture, occurs in
the arteries. The blood stasis caused by atrial
fibrillation may also cause this type of thrombosis.

15. Causes
 There are three main causes of thrombosis:
hypercoagulability, injury to the endothelial cells of
the blood vessel wall and abnormal flow of the blood.
 Hypercoagulability, also known as thrombophilia,
refers higher levels of coagulation factors in the blood
that increase susceptibility to thrombosis. This is
usually as a result of genetics or disorders of the
immune system.
 Injury to the epithelial cells on the wall of blood
vessels after trauma, surgery or and infection can also
precipitate coagulation and possible thrombosis.

16. Mechanism of thrombosis
 Platelets adhere to endothelium
forming a projecting mass
 Liberation of thromboplastins
from platelet aggregate leads to
initiate coagulation cascade
 Blood clot formation occurs

17. Thrombotic and antithrombotic
mechanisms
 Thrombotic
Thromboplastin
Factor V
PAF
vWF
 Anti-thrombotic
Thrombomodulin
Anti thrombin III
Alpha 2 macroglobulin
tPA
Normally these two groups are finely balanced to prevent thrombus formation. Damage
to endothelium however will favour thrombosis.
Most significant in arterial thrombosis

18.  Endothelial cells loss
 Atheromatous plaques: ulceration
 Damage by surgery
 Arteritis
 Indwelling vascular catheters
 Infusion of sclerosing chemicals
 Hydrodynamic forces
 Prolong hypertension
 Turbulance
 Toxins and immune mediated damage
 Bacterial toxins
 Cigarette smoke
 Immune mediatd: transplant rejection, immune complex
disease
 Radiation

19. Complications
 A common complication of thrombosis is hypoxia, due
to the obstruction of the artery of vein. When the
majority of the blood vessel is blocked, the oxygen
supply to the body is reduced and results in increased
production of lactic acid.

20. Prevention and Treatment As stasis of the blood is associated with increased risk
of thrombosis, it is important that movements are
made regularly, particularly if susceptible individuals
are likely to be sedentary for long periods of time, such
as in bed or on an airplane.
 For people at high risk of venous thromboembolism,
heparin can be administered to reduce risk of
pulmonary embolism, although this is associated with
higher susceptibility to bleeding due to the reduced
efficacy of the clotting factors. Therefore, heparin
offers greater use in the treatment, rather than
prevention of thrombosis.

21.  A more coherent method to prevent the formation of
deep vein thrombosis is the use of compression
stockings, which mechanically support the vein to
inhibit the formation of blood clots. This is
particularly beneficial as there are few side effects.
 Anticoagulants may increase the risk of major
bleeding slightly, but has been found to offer a benefit
in both the prevention and treatment of thrombosis

22. SHOCK
 is a life-threatening medical condition of low
blood perfusion to tissues resulting in cellular injury
and inadequate tissue function. The typical signs of
shock are low blood pressure,rapid heart rate, signs of
poor end-organ perfusion (i.e.: low urine output,
confusion, or loss of consciousness), and weak pulses.

23. Signs and symptoms
 The presentation of shock is variable with some people
having only minimal symptoms such as confusion and
weakness. While the general signs for all types of
shock are low blood pressure, decreased urine output,
and confusion, these may not always be present.While
a fast heart rate is common, those on β-blockers, those
who are athletic and in 30% of cases those with shock
due to intra abdominal bleeding may have a normal or
slow heart rate.

24. TYPES of SHOCK
CARDIOGENIC: (Acute, Chronic Heart Failure)
HYPOVOLEMIC: (Hemorrhage or Leakage)
SEPTIC: (“ENDOTOXIC” shock, #1 killer in ICU)
 NEUROGENIC: (loss of vascular tone)
 ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased
vascular permeability)

25. CARDIOGENIC shock
 MI
 VENTRICULAR RUPTURE
 ARRHYTHMIA
 CARDIAC TAMPONADE
 PULMONARY EMBOLISM (acute RIGHT heart
failure or “cor pulmonale”)

26. HYPOVOLEMIC shock
 HEMORRHAGE, Vasc. compartmentH2O
 VOMITING, Vasc. compartmentH2O
 DIARRHEA, Vasc. compartmentH2O
 BURNS, Vasc. compartmentH2O

27. SEPTIC shock
 OVERWHELMING INFECTION
 “ENDOTOXINS”, i.e., LPS (Usually Gm-)
 Gm+
 FUNGAL
 “SUPERANTIGENS”, (Superantigens are polyclonal T-lymphocyte
activators that induce systemic inflammatory cytokine cascades
similar to those occurring downstream in septic shock, “toxic
shock” antigents by staph are the prime example.)

28. CLINICAL STAGES of shock
NON-PROGRESSIVE
PROGRESSIVE
IRREVERSIBLE

29. CLINICAL STAGES of shock
NON-PROGRESSIVE
PROGRESSIVE
IRREVERSIBLE

30. NON-PROGRESSIVE
COMPENSATORY MECHANISMS
CATECHOLAMINES
VITAL ORGANS PERFUSED

31. PROGRESSIVE
HYPOPERFUSION
EARLY “VITAL” ORGAN FAILURE
OLIGURIA
ACIDOSIS

32. IRREVERSIBLE
HEMODYNAMIC
CORRECTIONS of
no use