Thromboembolism and shock Flashcards
(clot in original position):
Precedent of everything formation of inappropriate blood clot
Thrombosis
(clot in circulation): Can obstruct a
vessel where it will lodge can cause ischemia
to the surrounding tissue being supplied by
that vessel leading to infarction
Embolism
Circulatory failure part of
hemodynamic disorder with unique
characteristics but sometimes overlaps with
symptoms of thromboembolic disease
Shock
is one of the scourges of modern
man, because it underlies the most serious and
common forms of cardiovascular disease.
Thrombosis
If there is embolism in the lungs particularly in the
pulmonary vein, there will be________
pulmonary infarction.
Virchow’s triad: Endothelial Injury can cause ____
abnormal
blood flow and hypercoagulability
Virchow’s triad: Abnormal Blood Flow can lead to or
cause _____
endothelial injury and
hypercoagulability
T or F
Hypercoagulability does NOT cause
either endothelial injury or abnormal
blood flow
T
Injury to the endothelium leads to ______ (inhibited by aspirin)
Platelet activation
When there is endothelial injury, it exposes the
endothelium to _________ which leads to platelet activation.
Von Willebrand factor and tissue
factor
Causes of Endothelial injury
o Physical Injury o Infection o Abnormal Blood Flow o Inflammatory mediators o Metabolic Abnormalities o Toxins from cigarette smoke
This triggers Endothelial activation or dysfunction
that shifts the pattern of gene expression in
endothelium to _______
prothrombotic.
The 2 Prothrombotic Alterations
o Procoagulant changes
o Antifibrinolytic effects
In procoagulant changes, there is downregulation of thrombomodulin, as well as _________ and _____
Protein C and TFPI
In antifibrinolytic effects, Activated endothelial cells
secretes _________which
downregulates t-PA and limits
fibrinolysis
plasminogen activator
inhibitors (PAIs)
normal flow of blood in the
vessels is known as
laminar flow
T or F
Laminar flow
allows the red cells to travel centrally in the blood
vessels and plasma in the outer portion to prevent
the red cells from having contact with the
endothelium.
T
Blood flow can be altered in 2 ways:
Turbulence
Stasis
▪ Contributes to arterial and
cardiac thrombosis by causing endothelial injury
▪ Also forming little pockets of countercurrents that contribute to stasis
Turbulence
▪ Allows development of venous thrombi
Stasis
-Refers to an abnormally high tendency of the
blood to clot, typically caused by alterations in
coagulation factors
- important in venous thrombosis
HYPERCOAGULABILITY
▪ also called Leiden mutation
▪ Arg to Gln substitution in amino acid residue 506
▪ 60% in patients with recurrent DVT
Factor V mutation (autosomal dominant) (2-15%)
In factor V mutation, Heterozygotes have a ____ increased relative
risk of venous thrombosis, and homozygotes
have a ____increase
fivefold; 50-fold
▪ Single nucleotide change (G20210A) in 3’-
untranslated region of prothrombin gene
Prothrombin gene mutation (1-2%)
In prothrombin gene mutation, there is Increased prothrombin that leads to a
procoagulant state and an almost _____
increased risk of venous thrombosis
threefold
▪ predisposes a patient to develop DVT in
adolescence and early adulthood
▪ Affected individuals typically present with venous
thrombosis and recurrent thromboembolism
beginning in adolescence or early adulthood.
Others: Deficiencies of anticoagulants (antithrombin III,
protein C or protein S)
Homocystenemia can be caused by inherited deficiency of ______
cystathione β-synthetase
Homocystenemia
can also be
acquired, causes include deficiency of vitamin
B6, B12, and folic acid.
Hypercoagulability seen with advancing age may
be due to reduced ______(promotes
platelets aggregation) production which leads to
thrombosis
endothelial PGI2
Life-threatening disorder that occurs following
administration of unfractionated heparin
HEPARIN INDUCED THROMBOCYTOPENIA (HIT)
SYNDROME
(HIT)
SYNDROME: Most common presentation:
Thrombocytopenia
(HIT)
SYNDROME: Most serious complication:
Thrombosis
(HIT)
SYNDROME: Sequelae
o necrosis of the skin
o gangrene of the limbs
o stroke
o myocardial infarction
(HIT)
SYNDROME: diagnosis
requires the demonstration of anti–
PF4-heparin antibodies
▪ Autoimmune disorder characterized by: o Presence of one or more antiphospholipid (aPL) autoantibodies o Venous or arterial thromboses, or pregnancy complications such as recurrent miscarriages, unexplained fetal death, and premature birth.
ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS)
manifests only hypercoagulable
state in the absence of other autoimmune
disorders
ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS): PRIMARY
- individuals with a well-defined
autoimmune disease, such as systemic lupus
erythematosus (lupus anticoagulant syndrome)
this brings about the development of APS
Secondary
ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS): Clinical presentations can include:
o pulmonary embolism (following lower o extremity venous thrombosis), o pulmonary hypertension (from recurrent subclinical pulmonary emboli), o valvular heart disease o stroke o bowel infarction o renovascular hypertension
Usually mural, frequently
occlusive -> sequelae; coronary,
cerebral femoral occlusion
ARTERIAL THROMBI
Grey-white; friable meshwork of
platelets admixed with fibrin, red
cells and degenerating leukocytes
ARTERIAL THROMBI
Red-blue; contain more enmeshed
red cells
VENOUS THROMBI
Arterial thrombi grows in a _____ manner
retrograde
Venous thrombi grows in the ___________
direction of blood
flow
- How do you distinguish an antemortem from a post
mortem clot?
Antemortem thrombosis contain lines of Zahn,
features that help distinguish them from postmortem clots.
Postmortem clots are gelatinous and have a dark-red
dependent portion where red cells have settled by gravity
and a yellow “chicken fat” upper portion, and are usually
not attached to the underlying vessel wall.
Thrombi on heart valves are called?
Ans: Vegetations (can be sterile or infected as in infective
endocarditis). There are vegetations or thrombi that are
formed on valves especially in SLE patients and they are
called libman sacks. (Endocarditis associated with SLE is
k/s libman sacks endocarditis).
Thrombi accumulate
additional platelets and fibrin.
Propagation
Thrombi dislodge and travel
to other sites in the vasculature.
Embolization
is the result of
fibrinolysis. Which can lead to the rapid
shrinkage and total disappearance of recent
thrombi. In contrast, the extensive fibrin
deposition and cross-linking in older thrombi
render them more resistant to lysis. This
distinction explains why therapeutic
administration of fibrinolytic agents such as tPA.
Dissolution
Older thrombi become organized by the in growth of o endothelial cells o smooth muscle cells o fibroblasts.
Organization and recanalization.
▪ WIDESPREAD THROMBOSIS within the
microcirculation that may be of sudden or
insidious onset.
DISSEMINATED INTRAVASCULAR COAGULATION
T or F
DISSEMINATED INTRAVASCULAR COAGULATION
-It is not a specific disease but rather a
complication of a large number of conditions
associated with systemic activation of thrombin.
T
Causes of DIC
o Obstetric complication
o Cancers
o Severe Traumas
o Sepsis
Detached intravascular solid, liquid or gaseous
mass that is carried by the blood from its point of
origin to a distant site, where it causes tissue
dysfunction or infarction
EMBOLISM
▪ Originate from DVT and the most common form
of thromboembolic disease.
PULMONARY EMBOLISM
when the embolus straddles
the pulmonary artery bifurcation
Saddle embolus
a venous embolus
passes through an interatrial or interventricular
defect and gains access to the systemic
circulation
Paradoxical embolism:
T or F
Embolic obstruction of medium arteries with
subsequent vascular rupture can result in
pulmonary hemorrhage and usually cause pulmonary infarction.
F
** but usually does not
cause pulmonary infarction.
T or F
Multiple emboli overtime may cause pulmonary
hypertension and right ventricular failure.
T
