Professional Documents
Culture Documents
Fatimah Eliana
XII
Tissue trauma
XIIa (H)
XI
Tissue factor
XIa (H)
(W) VII VIIa
(W) IX
IXa (H)
CA++
PF 3
VIII (W)
Common Pathway
(W) X
Xa (H)
(Next slide)
Common Pathway
Xa (H)
Ca++
PF 3
V (W)
(H) (F)
(W) Prothrombin
Thrombin
Ca++
Fibrinogen
CA++
Fibrin
(soluble)
(H)
XIIIa
Fibrin (insoluble)
XIII
Coagulation
Cascade
A series of conversions of
inactive proenzymes to
activated enzymes,
culminating in the
formation of thrombin
Thrombin then coverts the
soluble plasma protein
fibrinogen to insoluble
fibrous protein fibrin
Coagulation
Cascade
Intrinsic
Surface contact
Extrinsic
Tissue injury
Control of cascade to
prevent clotting elsewhere
Antithrombins
activated by
heparin like
molecules on
endothelial cells
Clinical
administration of
heparin minimizes
thrombosis
Proteins C and S
Vitamin K
dependent
Plasminogenplasmin system
Breaks down
fibrin and inhibits
its polymerization
Products of split
fibrin are
anticoagulants
Thrombus Formation
Arterial Thrombus
Venous Thrombus
Arterial
Venous
Neuropathic
Foot ulcers
Arterial Venous
Neuropathic
Location
Distal Medial
malleolus point
Arterial disease
and risk factors for
atherosclerosis
Yes
No
No
Contra-lateral
pulses
No
Yes
Yes (maybe)
Skin changes of
venous HTN
No
Yes
No
Maybe No
Yes
Neuropathy
Pressure
DEEP VENOUS
THROMBOSIS
Definition
Etiology
Virchow triad
Venous stasis
Hypercoagulability
Inherited disorders of
coagulation
deficiency of protein S
deficiency protein C
deficiency antithrombin III.
Acquired disorders of
coagulation
Acquired disorders of
coagulation
also
predispose
to
thrombosis,
presumably due to hypercoagulability
Endothelial Injury
Clinical Pathophysiology
Clinical Pathophysiology
SCORE
Active cancer (treatment ongoing, or within 6 months or
palliative)
Diagnostic Studies
INR:
useful
for
guiding
the
management of patients with known
DVT who are on warfarin (Coumadin)
D-dimer
D-dimer
False-positive
patients:
D-dimers
occur
in
Imaging Studies
Invasive
Venography
Radiolabeled fibrinogen.
Noninvasive
Ultrasound with Doppler
Plethysmography
MRI techniques
Venography
Side Effects:
phlebitis
anaphylaxis
Venography
Nuclear Medicine
Studies
Because the
radioactive isotope
incorporates into a
growing thrombus,
this test can
distinguish new
clot from an old
clot
Plethysmography
Plethysmography
measures change
in lower extremity
volume in
response to
certain stimuli.
Ultrasonography
inexpensive,
noninvasive,
widely available
can also distinguish other causes of leg
swelling, such as tumor, popliteal cyst,
abscess, aneurysm, or hematoma.
Ultrasonography
Clinical limitations
Reader dependent
Duplex scans are less likely
to detect non-occluding
thrombi.
During the second half of
pregnancy, US becomes
less specific, because the
gravid uterus compresses
the inferior vena cava,
thereby changing Doppler
flow in the lower extremities
Magnetic Resonance
Imaging
Differential Diagnosis
Cellulitis
Thrombophlebitis
Arthritis
Asymmetric peripheral edema secondary
to CHF, liver disease, renal failure, or
nephrotic syndrome
Lymphangitis, Lymphedema
Extrinsic compression of iliac vein
secondary to tumor, hematoma, or
abscess
Differential Diagnosis
Hematoma
Muscle or soft tissue injury
Neurogenic pain
Postphlebitic syndrome
Prolonged immobilization or limb paralysis
Ruptured Baker cyst
Stress fractures or other bony lesions
Varicose veins
Management
Management
Management
Anticoagulation
Thrombolytic therapy for DVT
Surgery for DVT
Filters for DVT
Compression stockings
Anticoagulation
Anticoagulation
Anticoagulation
Anticoagulation
The
hemorrhagic
complications
attributed to heparin are thought to
arise from the larger higher molecular
weight fragments.
Anticoagulation
Advantages of Low-Molecular-Weight
Heparin Over Standard Unfractionated
Heparin
Superior bioavailability
Superior or equivalent safety and efficacy
Subcutaneous once- or twice-daily dosing
No laboratory monitoring
Less thrombocytopenia
Low-Molecular-Weight
Heparin
Warfarin
Thrombolytic therapy
for DVT
Advantages include:
Thrombolytic therapy
Thrombolytic therapy
Indication:
when
anticoagulant
therapy
is
ineffective, unsafe, contraindicated .
Controversial indications:
DVT with contraindication to
anticoagulation
DVT in patients with pre-existing
pulmonary hypertension
Free floating thrombus in proximal vein
Failure of existing filter device
Post pulmonary embolectomy
Compression stockings
(routinely recommended
Complications
Prophylaxis
ARTERY THROMBOSIS
Arterial Thrombus
Arterial thrombosis
angiographic picture
Severe arterial
thrombosis
Thrombus in left
atrium
Bacterial endocarditis
External iliac
Superficial femoral
Tibial
Antiplatelet Drugs
Aspirin,
Dipyridamole
(Persantine),
Ticlopidine (Ticlid) abciximab (ReoPro),
tirofiban (Aggrastat)
Action: prevent thrombosis in the
arteries
by
suppressing
platelet
aggregation
Use:
Prevention of MI, stroke for patient with
family history, DM
Prevention of repeat MI, stroke in patient
having TIA
Antiplatelet Drugs
Thrombolytic
.Thrombolytics
promote
fibrinolytic
mechanism (convert plasminogen to
plasmin and destroys the fibrin in the
clot)
Administering a thrombolytic drug
clot disintegrates
Side effects:
hemorrhage, allergic
reactions
Onset and peak are immediate and
rapid
Thrombolytic
Use :
Acute MI - within 4 hrs to dissolve clot
and unblock artery, so decrease
necrosis to myocardium.
Other uses:
pulmonary embolism
DVT
noncoronary arterial occlusion
Thrombolytic
Streptokinase,
Urokinase,
Tissue
plasminogen
activator
(t-PA),
anisoylated plasminogen streptokinase
activator complex (APSAC)
Streptokinase and Urokinase: enzymes
that act to convert plasminogen to
plasmin
t-PA and APSAC: activate plasminogen
by acting specifically on clot.
Aorto-bifemoral
bypass
CONCLUSION
VEIN
THROMBOSIAS
ARTERY
THROMBOSIS
Similar
name
Red thrombi
White thrombi
Contain
Higher concentration
of platetelts, lower
concentration of RBC
Prevention
Medication that
interrupt cloting
cascade
(anticoagulant)